The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The gene cact (CG5848) encodes the NF-kappa-B inhibitor protein Cactus in Drosophila melanogaster. This protein is the founding member and sole IκB-family inhibitor in the fruit fly, homologous to mammalian IκBα proteins (kaltschmidt2021thetranscriptionfactor pages 3-4, araujo2022chelonusinanitusbracovirus pages 17-19). Cactus belongs to the NF-kappa-B inhibitor family and contains characteristic ankyrin repeat domains (IPR002110, IPR036770) that mediate its interactions with Rel/NF-κB transcription factors (basith2013evolutionarystructuraland pages 11-12).
Cactus functions as a cytoplasmic inhibitor of NF-κB-family transcription factors, not as an enzyme, transporter, or receptor. Its primary molecular role is to bind and sequester the Rel-family transcription factors Dorsal (Dl) and Dorsal-related immunity factor (Dif) in the cytoplasm, preventing their nuclear translocation and thereby suppressing NF-κB-dependent gene transcription (kallstig2023theroleof pages 21-24, kaltschmidt2021thetranscriptionfactor pages 3-4, critchlow2024mappingthefunctional pages 2-4).
The interaction between Cactus and its substrates is mediated by six tandem ankyrin repeats (approximately 195–398 amino acids in related proteins) that form an ankyrin repeat domain (ARD) (araujo2022chelonusinanitusbracovirus pages 17-19, basith2013evolutionarystructuraland pages 11-12, araujo2022chelonusinanitusbracovirus pages 14-17). This ARD binds specifically to the Rel-homology domain (RHD) of Dorsal and Dif, with a reported dissociation constant of approximately 1.95 × 10⁻⁷ M for the Cactus–Dorsal interaction (bitra2012polydnavirusankproteins pages 2-3). The ankyrin repeats provide a curved, helical scaffold with exposed finger loops that determine binding specificity among different NF-κB proteins (basith2013evolutionarystructuraland pages 11-12).
Recent research has revealed that Cactus has a dual, context-dependent regulatory function rather than acting solely as an inhibitor (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 15-16). In regions without active Toll signaling, Cactus binds free Dorsal and prevents its Toll-independent nuclear entry, maintaining low basal NF-κB activity (barros2021areactiondiffusionnetwork pages 8-9). However, in ventral embryonic regions with strong Toll activation, Cactus-bound Dorsal complexes participate in Toll-responsive signaling and actually promote efficient signal-dependent nuclear translocation (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 15-16, barros2021areactiondiffusionnetwork pages 8-9).
This dual role is spatially regulated: reducing Cactus levels increases direct Dorsal nuclear import in dorsal and lateral regions while simultaneously decreasing Toll-dependent import in ventral regions, demonstrating that Cactus both inhibits basal activity and enables efficient Toll signaling (barros2021areactiondiffusionnetwork pages 8-9).
Cactus activity is controlled through signal-dependent phosphorylation and proteasomal degradation. Upon Toll pathway activation by the ligand Spätzle, signaling proceeds through the adaptor protein MyD88, the kinases Tube and Pelle (Drosophila IRAK homolog), leading to N-terminal phosphorylation of Cactus (kallstig2023theroleof pages 21-24, barros2021areactiondiffusionnetwork pages 6-8). Phosphorylated Cactus is then ubiquitinated and targeted for proteasomal degradation, which dissociates the Dorsal–Cactus complex and permits Dorsal nuclear translocation (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 6-8, barros2021areactiondiffusionnetwork pages 1-2).
In addition to Toll-dependent regulation, Cactus is subject to Toll-independent turnover mechanisms. The C-terminal PEST domain of Cactus is phosphorylated by casein kinase II (CKII), including at Ser468, which regulates its stability (barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 23-24). The calcium-dependent protease Calpain A also mediates limited proteolysis of Cactus, providing an alternative degradation pathway linked to maternal Dpp/BMP signaling (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 17-19).
Cactus functions primarily in the cytoplasm, where it binds and retains Dorsal and Dif outside the nucleus (barros2021areactiondiffusionnetwork pages 1-2, barros2021areactiondiffusionnetwork pages 19-20, barros2021areactiondiffusionnetwork pages 2-3). In the absence of Toll signaling, cytoplasmic Cactus forms stable Dorsal–Cactus complexes (DlC) that prevent Dorsal nuclear entry (barros2021areactiondiffusionnetwork pages 1-2, barros2021areactiondiffusionnetwork pages 6-8). Upon Toll activation, these complexes associate with membrane-associated Toll receptors to form DlCT signaling complexes, where Cactus and Dorsal are phosphorylated and released (barros2021areactiondiffusionnetwork pages 6-8).
While Cactus has been observed in nuclei of certain Drosophila tissues, its primary embryonic function is cytoplasmic regulation of Dorsal localization (barros2021areactiondiffusionnetwork pages 15-16, barros2021areactiondiffusionnetwork pages 24-25). The cytoplasmic Dorsal–Cactus complexes are mobile and undergo facilitated diffusion through the syncytial embryo, serving as a carrier mechanism that redistributes Dorsal toward regions of active Toll signaling (mcgehee2024mechanismsforcontrolling pages 2-3, schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 1-3).
Cactus is the central negative regulator of the Toll signaling pathway in Drosophila (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 1-2, barros2021areactiondiffusionnetwork pages 19-20). The Toll pathway operates in two major biological contexts:
1. Embryonic Development: During dorsal-ventral patterning, spatially restricted Toll activation creates a gradient of Cactus degradation that generates the nuclear Dorsal gradient essential for proper embryonic axis specification (barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 23-24, barros2021areactiondiffusionnetwork pages 17-19).
2. Innate Immunity: In larval and adult flies, microbial infection activates Toll receptors, leading to Cactus degradation and nuclear translocation of Dif and Dorsal, which activate antimicrobial peptide (AMP) gene expression (kallstig2023theroleof pages 21-24, critchlow2024mappingthefunctional pages 2-4). Cactus depletion results in constitutive activation of AMPs, increased hemocyte proliferation, and enhanced immune responses, demonstrating its role in limiting and resolving immune activation (critchlow2024mappingthefunctional pages 2-4, critchlow2024mappingthefunctional pages 4-6).
While Cactus primarily regulates the Toll pathway, recent studies have identified interactions with other signaling systems. In tumor models, Cactus can act downstream of the Hippo pathway effector Yorkie and upstream of JNK signaling, revealing context-dependent roles beyond canonical NF-κB inhibition (snigdha2020theykicactus(ikbα)jnk pages 19-29, snigdha2020theykicactus(ikbα)jnk pages 9-12, snigdha2020theykicactus(ikbα)jnk pages 12-16). However, Cactus does not directly regulate the IMD pathway, which uses the distinct NF-κB factor Relish that contains its own C-terminal ankyrin repeat inhibitory domain (kallstig2023theroleof pages 21-24).
Cactus plays an essential maternally supplied role in establishing the dorsal-ventral axis of the Drosophila embryo (barros2021areactiondiffusionnetwork pages 1-2, barros2021areactiondiffusionnetwork pages 23-24, mcgehee2024mechanismsforcontrolling pages 6-6). The spatial gradient of Cactus degradation, driven by ventrally localized Toll activation, generates the nuclear Dorsal gradient that specifies distinct tissue fates: ventral mesoderm (high nuclear Dorsal), lateral neuroectoderm (intermediate Dorsal), dorsal ectoderm (low Dorsal), and amnioserosa (no nuclear Dorsal) (barros2021areactiondiffusionnetwork pages 15-16, barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 1-2).
Key developmental target genes whose expression boundaries are controlled by the Cactus-regulated Dorsal gradient include snail and short gastrulation (sog) (barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 9-11). Altered Cactus dosage disrupts the precision and position of these expression domains, demonstrating its critical role in developmental patterning (barros2021areactiondiffusionnetwork pages 9-11).
A major recent advance in understanding Cactus function is the discovery of its role in morphogen shuttling through facilitated diffusion (mcgehee2024mechanismsforcontrolling pages 2-3, schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 1-3, schloop2020mechanismandimplications pages 1-2). In the syncytial embryo, mobile Dorsal–Cactus complexes diffuse through the shared cytoplasm with an estimated diffusion coefficient of 0.2–0.5 μm²/s (carrell2016afacilitateddiffusion pages 1-3, barros2021areactiondiffusionnetwork pages 17-19). Ventral Toll activation creates a "sink" by degrading Cactus, which drives net movement of Dorsal–Cactus complexes toward the ventral region (schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 5-7).
This shuttling mechanism explains how Cactus concentrates total Dorsal (both cytoplasmic and nuclear) on the ventral side of the embryo, enhancing the robustness of the Dorsal gradient and enabling proper development even in embryos with reduced Dorsal dosage (schloop2020mechanismandimplications pages 1-2, carrell2016afacilitateddiffusion pages 1-3).
In the innate immune system, Cactus restrains Toll-dependent activation of Dif and Dorsal, preventing inappropriate or excessive immune responses (kallstig2023theroleof pages 21-24, critchlow2024mappingthefunctional pages 2-4). Upon microbial challenge, Cactus degradation permits nuclear entry of these transcription factors, which activate expression of antimicrobial peptides and other immune effectors (critchlow2024mappingthefunctional pages 2-4, critchlow2024mappingthefunctional pages 4-6).
Studies in the red flour beetle Tribolium castaneum have quantitatively demonstrated that graded Cactus depletion increases AMP expression (including cecropin-2, defensin-2, and defensin-3), delays immune-response resolution, enhances infection resistance, but imposes fitness costs including reduced lifespan, fecundity, body mass, and gut integrity (critchlow2024mappingthefunctional pages 2-4, critchlow2024mappingthefunctional pages 4-6, critchlow2024mappingthefunctional pages 11-12). These findings establish Cactus as a key regulator of immune homeostasis and the trade-off between immune investment and organismal fitness.
Emerging research has identified context-dependent roles for Cactus in Drosophila tumor models. In RasV12; scribble-deficient carcinoma models, Cactus and Dorsal show elevated and heterogeneous expression, with Dorsal acting as the primary tumor-promoting factor by suppressing differentiation, blocking apoptosis, and promoting invasion through epithelial-mesenchymal transition factors Snail and Twist (brutscher2025activationofthe pages 4-6, dillard2024oncogenicrasdrivendorsalnfκb pages 11-14, brutscher2025activationofthe pages 6-7).
In Yorkie-activated, polarity-deficient tumors, Cactus accumulates downstream of Yorkie/Scalloped signaling and acts upstream of JNK to promote tumor growth and invasion (snigdha2020theykicactus(ikbα)jnk pages 19-29, snigdha2020theykicactus(ikbα)jnk pages 9-12, snigdha2020theykicactus(ikbα)jnk pages 1-5). Cactus depletion in these models reduces phosphorylated JNK, matrix metalloproteinase-1 (MMP1) expression, and invasive behavior (snigdha2020theykicactus(ikbα)jnk pages 9-12, snigdha2020theykicactus(ikbα)jnk pages 5-9, snigdha2020theykicactus(ikbα)jnk pages 12-16). This reveals an alternative, tumor-promoting function for Cactus distinct from its canonical NF-κB inhibitory role.
Cactus contains three major structural regions summarized in the table below:
| Domain/Region | Amino Acid Location (if known) | Structure | Function | Key Interactions |
|---|---|---|---|---|
| N-terminal signal-response region | N terminus; exact boundaries not established in the cited evidence | Regulatory region outside the ankyrin-repeat core; contains Toll-responsive phosphorylation and degradation determinants | Toll activation promotes phosphorylation followed by ubiquitination and proteasomal degradation of Cactus, releasing bound Dorsal for nuclear import. The responsible kinase is not definitively established; Pelle is implicated genetically and functionally in the pathway. (barros2021areactiondiffusionnetwork pages 6-8, barros2021areactiondiffusionnetwork pages 25-27, araujo2022chelonusinanitusbracovirus pages 17-19) | Toll-pathway signaling machinery; ubiquitination and proteasomal-turnover machinery; indirectly controls Dorsal release |
| Ankyrin-repeat domain (ARD) | Central region; six tandem ankyrin repeats, but exact D. melanogaster residue boundaries were not specified in the cited sources | Curved, repeat-based interaction scaffold built principally from alpha-helical ankyrin motifs; exposed finger loops are predicted to contribute to binding specificity. (araujo2022chelonusinanitusbracovirus pages 17-19, basith2013evolutionarystructuraland pages 11-12, araujo2022chelonusinanitusbracovirus pages 14-17) | Principal NF-kappa-B-binding module; binds Rel-family proteins and masks or functionally restrains their nuclear localization, thereby maintaining inactive cytoplasmic complexes. (basith2013evolutionarystructuraland pages 11-12, bitra2012polydnavirusankproteins pages 2-3) | Binds the Rel-homology region of Dorsal and also associates with Dif; purified Cactus ARD bound Dorsal with a reported dissociation constant of approximately 1.95 × 10^-7 M. (kallstig2023theroleof pages 21-24, sun2016βarrestinsnegativelyregulate pages 11-11, bitra2012polydnavirusankproteins pages 2-3) |
| Ankyrin finger-loop surfaces | Inter-repeat loops within the six-repeat ARD | Relatively flexible, solvent-exposed loops projecting from the more rigid helical scaffold | Likely determine partner recognition and specificity among NF-kappa-B/Rel proteins; repeat-by-repeat contacts with Dorsal have not been resolved experimentally in the cited evidence. (basith2013evolutionarystructuraland pages 11-12) | Contribute to the ARD interface with Dorsal and Dif, although individual contacting residues remain undefined |
| C-terminal PEST region | C terminus; includes Ser468 according to the cited CKII study | PEST-rich regulatory sequence expected to be comparatively flexible or disordered | Controls Cactus stability and Toll-independent turnover; casein kinase II phosphorylation at Ser468 and Calpain A-mediated limited proteolysis have been implicated in regulating Cactus abundance. (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 23-24, araujo2022chelonusinanitusbracovirus pages 17-19) | Casein kinase II, Calpain A, and regulatory factors that influence Cactus degradation |
| Full-length Cactus scaffold | Entire protein; UniProt Q03017 | Modular I-kappa-B-family protein combining terminal turnover-control regions with a central six-repeat interaction domain | Integrates stable binding of Dorsal and Dif with signal-responsive destruction. It therefore acts both as a cytoplasmic inhibitor and, in embryonic contexts, as a mobile carrier that supports Toll-dependent Dorsal redistribution and nuclear localization. (barros2021areactiondiffusionnetwork pages 2-3, schloop2020mechanismandimplications pages 1-2, carrell2016afacilitateddiffusion pages 1-3) | Dorsal-Cactus and Dif-Cactus complexes; Toll-responsive complexes; degradation machinery |
Table: Structural and regulatory regions of Drosophila Cactus, including its six-repeat ankyrin interaction domain and terminal turnover-control regions. The table distinguishes experimentally supported features from locations or contacts that remain unresolved.
The ankyrin repeat domain (six tandem repeats) forms the central functional unit, providing the binding interface for Dorsal and Dif (araujo2022chelonusinanitusbracovirus pages 17-19, basith2013evolutionarystructuraland pages 11-12, sun2016βarrestinsnegativelyregulate pages 11-11). The N-terminal signal-response region contains determinants for Toll-responsive phosphorylation and ubiquitination, enabling signal-dependent degradation (barros2021areactiondiffusionnetwork pages 6-8, barros2021areactiondiffusionnetwork pages 25-27, araujo2022chelonusinanitusbracovirus pages 17-19). The C-terminal PEST domain mediates Toll-independent regulation through CKII phosphorylation and Calpain A proteolysis (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 23-24, araujo2022chelonusinanitusbracovirus pages 17-19).
The comprehensive molecular functions and mechanisms of Cactus are summarized below:
| Molecular function | Mechanism/details | Binding partners | Key evidence/citations |
|---|---|---|---|
| Canonical IκB-family inhibitor | Cactus binds Rel-family transcription factors in the cytoplasm, restricting their nuclear localization and suppressing NF-κB-dependent transcription when Toll signaling is inactive. It is a regulatory scaffold, not an enzyme, transporter, or receptor. | Dorsal (Dl); Dorsal-related immunity factor (Dif) | Cytoplasmic Cactus–Dorsal complexes inhibit Dorsal nuclear entry; Cactus similarly restrains Dif during immune quiescence. (kallstig2023theroleof pages 21-24, kaltschmidt2021thetranscriptionfactor pages 3-4, critchlow2024mappingthefunctional pages 2-4) |
| Ankyrin-repeat-mediated recognition | Six tandem ankyrin repeats form the conserved ankyrin-repeat domain (ARD). Its helical scaffold and exposed loops provide the principal interaction surface for Rel/NF-κB proteins; the ARD binds the Rel-homology domain of Dorsal. | Dorsal RHD; Dif | Drosophila Cactus contains six ankyrin repeats, and an isolated Cactus ARD binds Dorsal with a reported dissociation constant of approximately 1.95 × 10⁻⁷ M. (araujo2022chelonusinanitusbracovirus pages 17-19, basith2013evolutionarystructuraland pages 11-12, bitra2012polydnavirusankproteins pages 2-3) |
| Toll-responsive molecular switch | Activated Spätzle–Toll signaling acts through MyD88, Tube, and Pelle and converts Cactus-bound Dorsal or Dif into transcriptionally active nuclear factors. Removal of Cactus permits their nuclear import. | Toll-pathway signaling complex; Dorsal; Dif | Toll activation culminates in Cactus removal and Dorsal/Dif nuclear translocation; Pelle is the Drosophila IRAK-family kinase associated with this regulatory step. (kallstig2023theroleof pages 21-24, barros2021areactiondiffusionnetwork pages 6-8, barros2021areactiondiffusionnetwork pages 25-27) |
| Phosphorylation, ubiquitination, and proteasomal degradation | Toll activation induces N-terminal phosphorylation of Cactus, followed by ubiquitination and proteasomal destruction. This dismantles inhibitory complexes and permits Dorsal nuclear accumulation. The precise direct kinase relationship is less completely resolved than the degradation sequence. | Dorsal; Pelle-associated machinery; ubiquitin–proteasome system | Evidence supports the sequence Toll activation → Cactus phosphorylation → ubiquitination → proteasomal degradation → Dorsal release. (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 6-8, barros2021areactiondiffusionnetwork pages 1-2) |
| Toll-independent turnover | Cactus abundance is also regulated through its C-terminal region. Casein kinase II phosphorylation of the PEST region, including reported Ser468 phosphorylation, and Calpain A-mediated proteolysis provide additional control over free Cactus and basal NF-κB activity. | Casein kinase II; Calpain A; Dpp/BMP-linked inputs | Toll-independent regulation links Cactus turnover to CKII, maternal Dpp/BMP signaling, and calcium-dependent Calpain A. (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 23-24) |
| Inhibition of basal Dorsal import | Away from strong Toll activity, Cactus binds free Dorsal and reduces Toll-independent nuclear entry. This keeps dorsal and lateral nuclear Dorsal concentrations low and sharpens embryonic transcriptional patterns. | Dorsal | Lowering Cactus increases free Dorsal and direct nuclear import, especially in dorsal and lateral embryonic regions. (barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 15-16) |
| Context-dependent promotion of Dorsal import | In ventral regions with strong Toll signaling, Cactus-bound Dorsal supplies Toll-responsive complexes that support efficient signal-dependent nuclear translocation. Reducing Cactus can therefore decrease ventral nuclear Dorsal while increasing basal import elsewhere. | Dorsal; activated Toll-associated complexes | Mutant analysis and reaction–diffusion modeling support inhibition of direct import dorsally but promotion of Toll-dependent import ventrally. (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 15-16) |
| Carrier-mediated shuttling | In the syncytial embryo, mobile Dorsal–Cactus complexes diffuse through the shared cytoplasm. Ventral Cactus degradation creates a sink that produces net ventral redistribution of Dorsal; released Dorsal is captured by nearby nuclei. | Dorsal; spatially activated Toll | Imaging and models support Cactus acting as a carrier that concentrates Dorsal ventrally. A modeled Dorsal–Cactus diffusion coefficient of approximately 0.2–0.5 μm²/s has been reported. (mcgehee2024mechanismsforcontrolling pages 2-3, schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 1-3, carrell2016afacilitateddiffusion pages 5-7, barros2021areactiondiffusionnetwork pages 17-19) |
| Regulation of developmental NF-κB output | By controlling nuclear Dorsal concentration and position, Cactus determines embryonic target-gene domains. Altered Cactus levels disturb expression boundaries such as those of snail and sog. | Dorsal; indirectly, Dorsal-responsive enhancers | Cactus-dependent changes in the Dorsal gradient alter snail and sog expression and specification of mesoderm, neuroectoderm, and dorsal ectoderm. (barros2021areactiondiffusionnetwork pages 1-2, mcgehee2024mechanismsforcontrolling pages 6-6, barros2021areactiondiffusionnetwork pages 9-11) |
| Regulation of immune NF-κB output | During infection, Cactus degradation releases principally Dif and Dorsal to activate antimicrobial-effector transcription. At rest and during resolution, Cactus limits the magnitude and duration of Toll-dependent immune-gene expression. | Dif; Dorsal; indirectly, antimicrobial-peptide promoters | Cactus loss or knockdown enhances antimicrobial-peptide expression and hemocyte proliferation, demonstrating negative regulation of Toll immune output. (kallstig2023theroleof pages 21-24, critchlow2024mappingthefunctional pages 2-4) |
| Feedback control and homeostasis | Dorsal activity can increase Cactus production or stability, creating negative feedback that replenishes the cytoplasmic inhibitor after activation and stabilizes developmental gradients. | Dorsal | Dorsal-dependent regulation of Cactus abundance is incorporated into quantitative models and supported by correlated Dorsal/Cactus expression. (barros2021areactiondiffusionnetwork pages 24-25, barros2021areactiondiffusionnetwork pages 1-2, brutscher2025activationofthe pages 4-6, dillard2024oncogenicrasdrivendorsalnfκb pages 11-14) |
Table: This table summarizes the experimentally supported and model-derived mechanisms by which Drosophila Cactus regulates Dorsal and Dif. It highlights its canonical inhibitory role, regulated degradation, ankyrin-mediated interactions, and context-dependent functions in NF-κB transport and signaling.
The biological processes and cellular contexts in which Cactus functions are detailed in this table:
| Biological process / cellular context | Role of Cactus | Key target genes / outputs | Tissue / developmental stage |
|---|---|---|---|
| Embryonic dorsal–ventral patterning | Cytoplasmic Cactus binds Dorsal and limits its nuclear entry. Spatially restricted Toll signaling promotes Cactus phosphorylation, ubiquitination, and degradation, generating the nuclear Dorsal gradient. Cactus can also facilitate Toll-dependent Dorsal import rather than acting solely as an inhibitor. (barros2021areactiondiffusionnetwork pages 15-16, barros2021areactiondiffusionnetwork pages 1-2, mcgehee2024mechanismsforcontrolling pages 6-6) | Concentration-dependent Dorsal targets include snail and sog; altered Cactus dosage changes the position and precision of their expression domains. (barros2021areactiondiffusionnetwork pages 8-9, barros2021areactiondiffusionnetwork pages 9-11) | Maternal and early syncytial embryo during establishment of the dorsal–ventral axis. (barros2021areactiondiffusionnetwork pages 23-24, mcgehee2024mechanismsforcontrolling pages 6-6) |
| Morphogen shuttling and gradient robustness | Mobile Dorsal–Cactus complexes undergo facilitated diffusion toward the ventral Toll-activation domain. Local Cactus degradation releases Dorsal for nuclear capture, making Cactus both an inhibitor and a carrier that concentrates Dorsal ventrally. (mcgehee2024mechanismsforcontrolling pages 2-3, schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 1-3) | Ventral enrichment of total and nuclear Dorsal and sharpening of the Dorsal gradient. A reaction–diffusion model estimated a Dorsal–Cactus diffusion coefficient of approximately 0.2–0.5 μm²/s. (schloop2020mechanismandimplications pages 1-2, carrell2016afacilitateddiffusion pages 5-7, barros2021areactiondiffusionnetwork pages 17-19) | Shared cytoplasm of the early syncytial embryo before cellularization. (mcgehee2024mechanismsforcontrolling pages 2-3, carrell2016afacilitateddiffusion pages 1-3) |
| Innate humoral immunity | Cactus restrains the Toll-responsive NF-κB factors Dif and Dorsal in the cytoplasm. Infection-induced Cactus degradation permits their nuclear entry; loss or silencing of Cactus increases and prolongs immune activation. (kallstig2023theroleof pages 21-24, critchlow2024mappingthefunctional pages 2-4) | Antimicrobial-peptide expression, hemolymph antibacterial activity, and immune-response magnitude and resolution; in D. melanogaster, Cactus loss is associated with increased AMP production and hemocyte proliferation. (critchlow2024mappingthefunctional pages 2-4) | Primarily larval and adult immune tissues, including fat body and hemocytes, during microbial challenge. (kallstig2023theroleof pages 21-24, critchlow2024mappingthefunctional pages 2-4) |
| Immune homeostasis and fitness trade-offs | By limiting and resolving Toll signaling, Cactus protects against excessive immune investment and immunopathology. Quantitative evidence from Tribolium castaneum—not D. melanogaster—shows that graded Cactus depletion can improve infection resistance while reducing lifespan, fecundity, body mass, and gut integrity. (critchlow2024mappingthefunctional pages 2-4, critchlow2024mappingthefunctional pages 4-6, critchlow2024mappingthefunctional pages 11-12) | AMP induction and decay, circulating hemocytes, infection survival, reproductive output, longevity, and gut homeostasis. (critchlow2024mappingthefunctional pages 4-6, critchlow2024mappingthefunctional pages 11-12) | Comparative whole-organism insect model following microbial challenge. (critchlow2024mappingthefunctional pages 4-6) |
| Ras/polarity-deficient carcinoma models | Toll–Dorsal signaling and Cactus expression are heterogeneous within tumors, including Dorsal-high/Cactus-high populations. Cactus is a pathway component and feedback-associated output, whereas Dorsal is the better-established causal driver of survival, impaired differentiation, and invasion. (dillard2024oncogenicrasdrivendorsalnfκb pages 11-14) | Elevated cact, PGRP-SA, and wntD; reduced retinal-determination gene eya; Dorsal-dependent invasion involving snail and twist. (brutscher2025activationofthe pages 4-6, dillard2024oncogenicrasdrivendorsalnfκb pages 11-14) | Ras^V12^; scribble-deficient epithelial and imaginal-disc tumor models. (brutscher2025activationofthe pages 4-6, dillard2024oncogenicrasdrivendorsalnfκb pages 11-14) |
| Yorkie/Hippo–JNK tumor signaling | In polarity-deficient tumors, Yorkie/Scalloped-dependent Cactus accumulation acts upstream of JNK. Cactus depletion reduces phosphorylated JNK, MMP1, clone growth, and invasion, revealing a context-specific tumor-promoting function distinct from canonical NF-κB inhibition. (snigdha2020theykicactus(ikbα)jnk pages 19-29, snigdha2020theykicactus(ikbα)jnk pages 9-12, snigdha2020theykicactus(ikbα)jnk pages 12-16) | Increased phospho-JNK and MMP1, basement-membrane remodeling, tumor growth, and invasive behavior. (snigdha2020theykicactus(ikbα)jnk pages 9-12, snigdha2020theykicactus(ikbα)jnk pages 1-5) | Larval imaginal-disc tumors driven by activated Yorkie or Ras together with impaired epithelial polarity. (snigdha2020theykicactus(ikbα)jnk pages 1-5, snigdha2020theykicactus(ikbα)jnk pages 5-9) |
| Toll-associated apoptosis and tissue homeostasis | Experimental Toll activation can promote reactive-oxygen-species production, JNK activity, and caspase-dependent death. Cactus regulates access to the activated Toll state through its inhibition of Dorsal/Dif, although a direct Cactus-specific apoptotic mechanism remains unestablished. (barros2021areactiondiffusionnetwork pages 1-2, snigdha2020theykicactus(ikbα)jnk pages 9-12) | ROS, activated JNK, caspase-dependent apoptosis, and altered tissue growth. (snigdha2020theykicactus(ikbα)jnk pages 9-12) | Developing Drosophila tissues under experimental or physiological Toll activation. (barros2021areactiondiffusionnetwork pages 1-2) |
Table: Summary of the developmental, immune, and tumor-associated contexts in which Drosophila melanogaster Cactus functions. The table distinguishes established fly mechanisms from comparative insect evidence.
Recent publications have advanced understanding of Cactus in several areas:
Quantitative immune regulation: The 2024 study by Critchlow et al. provided the first dose-response analysis of Cactus depletion, demonstrating that immune activation and fitness costs scale quantitatively with Cactus knockdown levels, revealing the functional form of immune-fitness trade-offs (critchlow2024mappingthefunctional pages 2-4, critchlow2024mappingthefunctional pages 4-6).
Tumor signaling networks: The 2024-2025 studies by Dillard et al. and Brutscher et al. established that oncogenic Ras drives Dorsal/NF-κB signaling in carcinoma models, with Cactus as both a pathway component and transcriptional target (dillard2024oncogenicrasdrivendorsalnfκb pages 11-14, brutscher2025activationofthe pages 6-7).
Dual regulatory mechanisms: The 2021 computational study by Barros et al. and the 2024 review by McGehee and Stathopoulos synthesized evidence for Cactus's dual role in both inhibiting and promoting Dorsal nuclear localization, depending on spatial context and Toll activity (barros2021areactiondiffusionnetwork pages 2-3, barros2021areactiondiffusionnetwork pages 8-9, mcgehee2024mechanismsforcontrolling pages 2-3).
Spatiotemporal dynamics: The 2020 and 2016 studies on facilitated diffusion established Cactus as a morphogen carrier, not just an inhibitor, with quantitative estimates of diffusion coefficients and transport mechanisms (schloop2020mechanismandimplications pages 2-3, carrell2016afacilitateddiffusion pages 1-3, carrell2016afacilitateddiffusion pages 5-7).
The Cactus protein and its regulatory mechanisms are highly conserved across arthropods and represent the ancestral IκB-NF-κB regulatory system (kaltschmidt2021thetranscriptionfactor pages 3-4, barros2021areactiondiffusionnetwork pages 24-25). The six-ankyrin-repeat architecture and Toll-responsive degradation pathway have been identified in crustaceans (shrimp) and other insects, demonstrating broad conservation of this regulatory module (li2012identificationcharacterizationand pages 5-7, sun2016βarrestinsnegativelyregulate pages 11-11).
Cactus (encoded by the cact gene, UniProt Q03017) is the sole IκB-family NF-κB inhibitor in Drosophila melanogaster and functions as a multifaceted regulator of Rel/NF-κB transcription factors. Its primary molecular function is to bind Dorsal and Dif via six ankyrin repeats, sequestering them in the cytoplasm and preventing nuclear translocation. However, Cactus also serves as a mobile carrier that redistributes Dorsal through facilitated diffusion and promotes efficient Toll-dependent nuclear import in regions of active signaling.
Cactus is essential for embryonic dorsal-ventral patterning, where it controls the nuclear Dorsal gradient that specifies tissue fates, and for innate immunity, where it restrains and resolves Toll-dependent antimicrobial responses. Its activity is regulated through signal-dependent N-terminal phosphorylation and proteasomal degradation, as well as Toll-independent C-terminal PEST domain modifications by CKII and Calpain A.
Recent studies (2020-2025) have revealed Cactus's dual regulatory roles, quantified immune-fitness trade-offs, established its function as a morphogen carrier, and identified context-dependent tumor-promoting activities. The structural basis for its function resides in the six-ankyrin-repeat domain that binds NF-κB proteins, coupled with regulatory N- and C-terminal regions that integrate multiple signaling inputs to control its stability and activity. This makes Cactus a paradigmatic example of an IκB-family regulator with conserved and context-dependent functions across development, immunity, and disease.
References
(kaltschmidt2021thetranscriptionfactor pages 3-4): Christian Kaltschmidt, Johannes F. W. Greiner, and Barbara Kaltschmidt. The transcription factor nf-κb in stem cells and development. Cells, 10:2042, Aug 2021. URL: https://doi.org/10.3390/cells10082042, doi:10.3390/cells10082042. This article has 125 citations.
(araujo2022chelonusinanitusbracovirus pages 17-19): Alexandra Cerqueira de Araujo, Thibaut Josse, Vonick Sibut, Mariko Urabe, Azam Asadullah, Valérie Barbe, Madoka Nakai, Elisabeth Huguet, Georges Periquet, and Jean-Michel Drezen. Chelonus inanitus bracovirus encodes lineage-specific proteins and truncated immune iκb-like factors. Oct 2022. URL: https://doi.org/10.1099/jgv.0.001791, doi:10.1099/jgv.0.001791. This article has 4 citations and is from a peer-reviewed journal.
(basith2013evolutionarystructuraland pages 11-12): Shaherin Basith, Balachandran Manavalan, Vijayakumar Gosu, and Sangdun Choi. Evolutionary, structural and functional interplay of the iκb family members. PLoS ONE, 8:e54178, Jan 2013. URL: https://doi.org/10.1371/journal.pone.0054178, doi:10.1371/journal.pone.0054178. This article has 30 citations and is from a peer-reviewed journal.
(kallstig2023theroleof pages 21-24): The role of the NF-kappaB pathway in Amyotrophic lateral sclerosis pathogenesis This article has 1 citations.
(critchlow2024mappingthefunctional pages 2-4): Justin T. Critchlow, Arun Prakash, Katherine Y. Zhong, and Ann T. Tate. Mapping the functional form of the trade-off between infection resistance and reproductive fitness under dysregulated immune signaling. PLOS Pathogens, Feb 2024. URL: https://doi.org/10.1371/journal.ppat.1012049, doi:10.1371/journal.ppat.1012049. This article has 12 citations and is from a highest quality peer-reviewed journal.
(araujo2022chelonusinanitusbracovirus pages 14-17): Alexandra Cerqueira de Araujo, Thibaut Josse, Vonick Sibut, Mariko Urabe, Azam Asadullah, Valérie Barbe, Madoka Nakai, Elisabeth Huguet, Georges Periquet, and Jean-Michel Drezen. Chelonus inanitus bracovirus encodes lineage-specific proteins and truncated immune iκb-like factors. Oct 2022. URL: https://doi.org/10.1099/jgv.0.001791, doi:10.1099/jgv.0.001791. This article has 4 citations and is from a peer-reviewed journal.
(bitra2012polydnavirusankproteins pages 2-3): Kavita Bitra, Richard J. Suderman, and Michael R. Strand. Polydnavirus ank proteins bind nf-κb homodimers and inhibit processing of relish. PLoS Pathogens, 8:e1002722, May 2012. URL: https://doi.org/10.1371/journal.ppat.1002722, doi:10.1371/journal.ppat.1002722. This article has 96 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 2-3): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 8-9): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 15-16): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 6-8): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 1-2): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 24-25): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 23-24): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 17-19): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(barros2021areactiondiffusionnetwork pages 19-20): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(mcgehee2024mechanismsforcontrolling pages 2-3): James McGehee and Angelike Stathopoulos. Mechanisms for controlling dorsal nuclear levels. Frontiers in Cell and Developmental Biology, Aug 2024. URL: https://doi.org/10.3389/fcell.2024.1436369, doi:10.3389/fcell.2024.1436369. This article has 1 citations.
(schloop2020mechanismandimplications pages 2-3): Allison E. Schloop, Sophia Carrell-Noel, Jeramey Friedman, Alexander J. Thomas, and Gregory T. Reeves. Mechanism and implications of morphogen shuttling: lessons learned from dorsal and cactus in drosophila. May 2020. URL: https://doi.org/10.1016/j.ydbio.2020.01.011, doi:10.1016/j.ydbio.2020.01.011. This article has 9 citations and is from a peer-reviewed journal.
(carrell2016afacilitateddiffusion pages 1-3): Sophia N. Carrell, Michael O'Connell, T. Jacobsen, Amy E. Pomeroy, S. M. Hayes, and Gregory T. Reeves. A facilitated diffusion mechanism establishes the drosophila dorsal gradient. Development, 144:4450-4461, Jun 2016. URL: https://doi.org/10.1101/057091, doi:10.1101/057091. This article has 30 citations and is from a domain leading peer-reviewed journal.
(critchlow2024mappingthefunctional pages 4-6): Justin T. Critchlow, Arun Prakash, Katherine Y. Zhong, and Ann T. Tate. Mapping the functional form of the trade-off between infection resistance and reproductive fitness under dysregulated immune signaling. PLOS Pathogens, Feb 2024. URL: https://doi.org/10.1371/journal.ppat.1012049, doi:10.1371/journal.ppat.1012049. This article has 12 citations and is from a highest quality peer-reviewed journal.
(snigdha2020theykicactus(ikbα)jnk pages 19-29): Kirti Snigdha, Amit Singh, and Madhuri Kango-Singh. The yki-cactus (ikbα)-jnk axis promotes tumor growth and progression in drosophila. bioRxiv, Aug 2020. URL: https://doi.org/10.1101/2020.08.16.253005, doi:10.1101/2020.08.16.253005. This article has 0 citations.
(snigdha2020theykicactus(ikbα)jnk pages 9-12): Kirti Snigdha, Amit Singh, and Madhuri Kango-Singh. The yki-cactus (ikbα)-jnk axis promotes tumor growth and progression in drosophila. bioRxiv, Aug 2020. URL: https://doi.org/10.1101/2020.08.16.253005, doi:10.1101/2020.08.16.253005. This article has 0 citations.
(snigdha2020theykicactus(ikbα)jnk pages 12-16): Kirti Snigdha, Amit Singh, and Madhuri Kango-Singh. The yki-cactus (ikbα)-jnk axis promotes tumor growth and progression in drosophila. bioRxiv, Aug 2020. URL: https://doi.org/10.1101/2020.08.16.253005, doi:10.1101/2020.08.16.253005. This article has 0 citations.
(mcgehee2024mechanismsforcontrolling pages 6-6): James McGehee and Angelike Stathopoulos. Mechanisms for controlling dorsal nuclear levels. Frontiers in Cell and Developmental Biology, Aug 2024. URL: https://doi.org/10.3389/fcell.2024.1436369, doi:10.3389/fcell.2024.1436369. This article has 1 citations.
(barros2021areactiondiffusionnetwork pages 9-11): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(schloop2020mechanismandimplications pages 1-2): Allison E. Schloop, Sophia Carrell-Noel, Jeramey Friedman, Alexander J. Thomas, and Gregory T. Reeves. Mechanism and implications of morphogen shuttling: lessons learned from dorsal and cactus in drosophila. May 2020. URL: https://doi.org/10.1016/j.ydbio.2020.01.011, doi:10.1016/j.ydbio.2020.01.011. This article has 9 citations and is from a peer-reviewed journal.
(carrell2016afacilitateddiffusion pages 5-7): Sophia N. Carrell, Michael O'Connell, T. Jacobsen, Amy E. Pomeroy, S. M. Hayes, and Gregory T. Reeves. A facilitated diffusion mechanism establishes the drosophila dorsal gradient. Development, 144:4450-4461, Jun 2016. URL: https://doi.org/10.1101/057091, doi:10.1101/057091. This article has 30 citations and is from a domain leading peer-reviewed journal.
(critchlow2024mappingthefunctional pages 11-12): Justin T. Critchlow, Arun Prakash, Katherine Y. Zhong, and Ann T. Tate. Mapping the functional form of the trade-off between infection resistance and reproductive fitness under dysregulated immune signaling. PLOS Pathogens, Feb 2024. URL: https://doi.org/10.1371/journal.ppat.1012049, doi:10.1371/journal.ppat.1012049. This article has 12 citations and is from a highest quality peer-reviewed journal.
(brutscher2025activationofthe pages 4-6): Fabienne Brutscher, Federico Germani, George Hausmann, Lena Jutz, and Konrad Basler. Activation of the drosophila innate immune system accelerates growth in cooperation with oncogenic ras. PLOS Biology, 23:e3003068, Apr 2025. URL: https://doi.org/10.1371/journal.pbio.3003068, doi:10.1371/journal.pbio.3003068. This article has 7 citations and is from a highest quality peer-reviewed journal.
(dillard2024oncogenicrasdrivendorsalnfκb pages 11-14): Caroline Dillard, Jose Teles Reis, Ashish Jain, Roland Le Borgne, Heinrich Jasper, and Tor Erik Rusten. Oncogenic ras-driven dorsal/nf-κb signaling contributes to tumorigenesis in a drosophila carcinoma model. bioRxiv, May 2024. URL: https://doi.org/10.1101/2024.05.08.593126, doi:10.1101/2024.05.08.593126. This article has 1 citations.
(brutscher2025activationofthe pages 6-7): Fabienne Brutscher, Federico Germani, George Hausmann, Lena Jutz, and Konrad Basler. Activation of the drosophila innate immune system accelerates growth in cooperation with oncogenic ras. PLOS Biology, 23:e3003068, Apr 2025. URL: https://doi.org/10.1371/journal.pbio.3003068, doi:10.1371/journal.pbio.3003068. This article has 7 citations and is from a highest quality peer-reviewed journal.
(snigdha2020theykicactus(ikbα)jnk pages 1-5): Kirti Snigdha, Amit Singh, and Madhuri Kango-Singh. The yki-cactus (ikbα)-jnk axis promotes tumor growth and progression in drosophila. bioRxiv, Aug 2020. URL: https://doi.org/10.1101/2020.08.16.253005, doi:10.1101/2020.08.16.253005. This article has 0 citations.
(snigdha2020theykicactus(ikbα)jnk pages 5-9): Kirti Snigdha, Amit Singh, and Madhuri Kango-Singh. The yki-cactus (ikbα)-jnk axis promotes tumor growth and progression in drosophila. bioRxiv, Aug 2020. URL: https://doi.org/10.1101/2020.08.16.253005, doi:10.1101/2020.08.16.253005. This article has 0 citations.
(barros2021areactiondiffusionnetwork pages 25-27): Claudio D. T. Barros, Maira A. Cardoso, Paulo M. Bisch, Helena M. Araujo, and Francisco J. P. Lopes. A reaction-diffusion network model predicts a dual role of cactus/iκb to regulate dorsal/nfκb nuclear translocation in drosophila. PLOS Computational Biology, 17:e1009040, May 2021. URL: https://doi.org/10.1371/journal.pcbi.1009040, doi:10.1371/journal.pcbi.1009040. This article has 7 citations and is from a highest quality peer-reviewed journal.
(sun2016βarrestinsnegativelyregulate pages 11-11): Jie-Jie Sun, Jiang-Feng Lan, Xiu-Zhen Shi, Ming-Chong Yang, Guo-Juan Niu, Ding Ding, Xiao-Fan Zhao, Xiao-Qiang Yu, and Jin-Xing Wang. Β-arrestins negatively regulate the toll pathway in shrimp by preventing dorsal translocation and inhibiting dorsal transcriptional activity. Journal of Biological Chemistry, 291:7488-7504, Apr 2016. URL: https://doi.org/10.1074/jbc.m115.698134, doi:10.1074/jbc.m115.698134. This article has 57 citations and is from a domain leading peer-reviewed journal.
(li2012identificationcharacterizationand pages 5-7): Chaozheng Li, Yi-Xiao Chen, Shuang Zhang, Ling Lü, Yi-Hong Chen, Jiaoting Chai, Shaoping Weng, Yong-Gui Chen, Jianguo He, and Xiaopeng Xu. Identification, characterization, and function analysis of the cactus gene from litopenaeus vannamei. PLoS ONE, 7:e49711, Nov 2012. URL: https://doi.org/10.1371/journal.pone.0049711, doi:10.1371/journal.pone.0049711. This article has 81 citations and is from a peer-reviewed journal.