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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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 nphp-2 (UniProt Q9BPN3; ORF Y32G9A.6/CELE_Y32G9A.6) encodes the Caenorhabditis elegans ortholog of mammalian Inversin (INVS/NPHP2), a protein causally linked to nephronophthisis type 2 (infantile nephronophthisis) in humans (OpenTargets Search: nephronophthisis-INVS, warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2). The assignment of Y32G9A.6 as the C. elegans inversin ortholog was confirmed through BLAST homology searches, the presence of an X-box promoter element (characteristic of ciliary genes regulated by the DAF-19 transcription factor), and conservation of key protein domains (warburtonpitt2015theciliopathygene pages 108-114, warburtonpitt2015theciliopathygene pages 104-108, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4). Importantly, nphp-2 is distinct from mlt-4, another C. elegans ankyrin repeat-containing protein that was also identified in BLAST searches but lacks the X-box promoter and many inversin-specific domains (warburtonpitt2015theciliopathygene pages 108-114, warburtonpitt2015theciliopathygene pages 104-108).
NPHP-2 is an ankyrin repeat domain-containing protein with a multi-domain architecture that mirrors its mammalian counterpart. Its key domains include:
The protein is not an enzyme, transporter, or signaling receptor; rather, it functions as a structural/adapter protein and genetic modifier that coordinates ciliary compartment organization through protein–protein interactions mediated by its ankyrin repeats and calcium-sensing EF-hand domain.
The nphp-2 gene encodes two protein isoforms: NPHP-2L (full-length, longer isoform) and NPHP-2S (shorter isoform lacking a 22 amino acid region) (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 108-114). Both are expressed in ciliated sensory neurons of C. elegans, including amphid and phasmid neurons (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4).
The subcellular localization of NPHP-2 is central to understanding its function:
This middle segment/InvC localization is distinct from most other ciliopathy-associated proteins (cystoproteins), which typically localize to the transition zone (warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4). The confinement of NPHP-2 to proximal ciliary subdomains is maintained by the transition zone barrier/ciliary zone of exclusion (CIZE), established by MKS-5/RPGRIP1L, which acts as a lipid gate restricting the diffusion of signaling proteins including NPHP-2 and GPCRs to distal ciliary domains (jensen2015formationofthe pages 1-2, jensen2015formationofthe pages 12-14).
NPHP-2 is not a component of the intraflagellar transport (IFT) machinery, and IFT velocities are not significantly affected by nphp-2 mutations (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8). Instead, NPHP-2 functions as a structural organizer of the ciliary middle segment and as a genetic nexus connecting multiple ciliopathy-related protein modules:
NPHP-2 is required for proper cilia formation, placement, and orientation. Loss of nphp-2 causes:
- Transition zone displacement and disorganization, with cilia dispersed over larger areas and anteriorly displaced phasmid cilia (warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4, warburtonpitt2015theciliopathygene pages 95-99).
- Dye-filling (Dyf) defects in phasmid neurons, indicating that cilia fail to properly contact the sensory pore (warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4, warburtonpitt2015theciliopathygene pages 95-99).
- Shortened phasmid dendrites (warburtonpitt2012ciliogenesisincaenorhabditis pages 8-9).
- In double mutants with nphp-4, severely compromised cilia with complete Dyf defects in both amphid and phasmid sensilla, demonstrating functional redundancy (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 95-99).
NPHP-2 is required for proper microtubule ultrastructure within cilia. In nphp-2 mutants, amphid channel cilia exhibit lengthwise shifts with asynchronous microtubule doublet B-tubules and disorganized Y-links at the transition zone (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 4-5). In arl-13; nphp-2 double mutants, most amphid channel cilia are absent, and those present show only microtubule singlets with abnormal transition zone microtubules (warburtonpitt2014thenphp2and pages 4-5).
NPHP-2 regulates tubulin glutamylation, a critical post-translational modification. Notably, glutamylation is not required for ciliary targeting of InvC or doublet region components; rather, glutamylation is modulated by nphp-2, arl-13, and unc-119 (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 1-2).
NPHP-2 is required for the correct localization of ciliary signaling proteins, including the cyclic nucleotide-gated channel subunits TAX-2 and TAX-4 to the proximal cilium/InvC (warburtonpitt2015theciliopathygene pages 29-33). NPHP-2 also regulates the ciliary localization of sensory signaling molecules in a cell-type-dependent manner (blacque2014compartmentswithina pages 7-8).
NPHP-2 participates in multiple redundant genetic networks:
NPHP-2 is partially redundant with NPHP-1 and NPHP-4 for cilia formation and transition zone placement in both amphid and phasmid neurons (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2015theciliopathygene pages 104-108, warburtonpitt2015theciliopathygene pages 95-99). The nphp-2; nphp-4 double mutant displays dramatically exacerbated ciliary defects compared to either single mutant (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 95-99). NPHP-2 physically interacts with NPHP-1 and NPHP-4, as well as with B9 domain proteins and MKS pathway components (warburtonpitt2015theciliopathygene pages 104-108, blacque2014compartmentswithina pages 7-8).
NPHP-2 genetically interacts with MKS pathway genes (mks-1, mks-3, mks-6, mksr-1, mksr-2) in a sensillum-specific manner to control cilia formation and placement (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2015theciliopathygene pages 104-108). The NPHP and MKS modules work redundantly to seal the ciliary compartment and establish transition zone barriers (cevik2013activetransportand pages 5-6).
NPHP-2 interacts with doublet region genes, forming two parallel redundant genetic modules: nphp-2 + klp-11 and arl-13 + unc-119, both of which are antagonized by HDAC-6 deacetylase and modulated by ARL-3 (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 1-2). These modules regulate cilia placement, ciliary microtubule ultrastructure, tubulin glutamylation, and the sizes of the NPHP-2/InvC and ARL-13/doublet region territories (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 1-2, warburtonpitt2014thenphp2and pages 4-5).
In mammals, inversin forms an Inversin complex (INV complex) with NEK8 and ANKS6 at the proximal ciliary shaft (beyrent2024dimerizationactivatesthe pages 1-2). In C. elegans, recent work by Beyrent et al. (2024) demonstrated that the C. elegans homologs MLT-4 (INVS), NEKL-2 (NEK8), and MLT-2 (ANKS6) form a tripartite Inversin complex that is activated by dimerization — dynamic switching between an inactive monomer and an active dimer gates complex output (beyrent2024dimerizationactivatesthe pages 1-2). However, NPHP-2/Y32G9A.6 is distinct from MLT-4; the initial BLAST analysis identified both as potential inversin homologs, but NPHP-2 was selected as the closer ortholog based on domain conservation and X-box promoter usage, while MLT-4 functions primarily in epidermal molting (warburtonpitt2015theciliopathygene pages 108-114, warburtonpitt2015theciliopathygene pages 104-108). The relationship between the NPHP-2 ciliary functions and the MLT-4/NEKL-2/MLT-2 Inversin complex remains an area of ongoing investigation.
Mammalian inversin has been proposed to act as a molecular switch between canonical Wnt/β-catenin and non-canonical Wnt/planar cell polarity (PCP) pathways by targeting cytoplasmic Dishevelled (Dvl) for degradation, thereby downregulating canonical Wnt signaling and promoting PCP signaling (veland2013inversinnephrocystin2isrequired pages 4-4, goggolidou2014wntandplanar pages 2-4, veland2013inversinnephrocystin2isrequired pages 1-2). Studies in inv⁻/⁻ mouse embryonic fibroblasts showed elevated β-catenin signaling, upregulation of Wnt target genes, and defective ciliary localization of Dvl-3, leading to impaired cell polarity and migration (veland2013inversinnephrocystin2isrequired pages 4-4, veland2013inversinnephrocystin2isrequired pages 12-13). However, this model has been challenged by more recent in vivo studies showing no upregulation of canonical Wnt signaling and no nuclear β-catenin accumulation in inv⁻/⁻ mice, leading to the conclusion that the role of inversin in Wnt signaling is now unclear (warburtonpitt2015theciliopathygene pages 40-44). Whether NPHP-2 plays a similar role in Wnt signaling in C. elegans has not been directly demonstrated; the C. elegans studies have focused primarily on ciliary structural and IFT-related functions rather than Wnt pathway regulation.
| Property | Summary |
|---|---|
| Gene name | nphp-2 (C. elegans); identified as the ciliary inversin/NPHP2 ortholog used in sensory-cilia studies, distinct from mlt-4 (warburtonpitt2015theciliopathygene pages 108-114, warburtonpitt2015theciliopathygene pages 104-108, warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8) |
| ORF name | Y32G9A.6 / CELE_Y32G9A.6 (matches the UniProt target context and literature assignment) (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4) |
| Mammalian ortholog | Ortholog of mammalian INVS/NPHP2 (inversin) (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8) |
| Human disease association | Human INVS/NPHP2 is associated with nephronophthisis type 2 / infantile nephronophthisis (OpenTargets Search: nephronophthisis-INVS) |
| Protein isoforms | Two isoforms are described: NPHP-2L (full-length) and NPHP-2S (shorter isoform lacking a 22 aa region) (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 108-114) |
| Domain structure | Conserved ankyrin repeat region, nuclear localization sequences (NLSs), destruction box (D-box), coil region, and predicted EF-hand Ca2+-binding domain; ankyrin repeats are a defining feature and EF-hand is functionally important in several cilia types (warburtonpitt2014thenphp2and pages 4-5, warburtonpitt2015theciliopathygene pages 108-114, warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2014thenphp2and pages 10-11) |
| Role of ankyrin repeats | Ankyrin-repeat region contributes to ciliary targeting, including evidence from AWB neurons (warburtonpitt2015theciliopathygene pages 29-33) |
| Role of EF-hand | EF-hand is required for robust ciliary localization and function in amphid channel and phasmid cilia; deletion causes faint/absent localization and poor rescue of mutant phenotypes, indicating Ca2+-dependent regulation (warburtonpitt2014thenphp2and pages 4-5, warburtonpitt2014thenphp2and pages 10-11) |
| Localization: NPHP-2L | Localizes mainly to the ciliary middle segment / Inversin compartment (InvC) of amphid and phasmid sensory cilia; this compartment is distinct from the transition zone (TZ) (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4, warburtonpitt2014thenphp2and pages 1-2) |
| Localization: NPHP-2S | Broader localization throughout the cell body, axon, dendrite, and cilium, while being excluded from the nucleus and transition zone (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 108-114) |
| Expression pattern | Expressed in ciliated sensory neurons of C. elegans (including amphid and phasmid neurons) (warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4) |
| Primary biological function | Functions in ciliogenesis, cilia placement/orientation, transition zone placement, and organization of the proximal ciliary shaft/Inv compartment rather than as a core IFT factor (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4, warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8, warburtonpitt2014thenphp2and pages 2-3) |
| Relationship to IFT | NPHP-2 is not required for gross IFT function; IFT velocities were not significantly altered in nphp-2 mutants, arguing its primary role is structural/organizational rather than IFT cargo transport (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8) |
| Key genetic interactions: NPHP module | Shows partially redundant interactions with nphp-1 and nphp-4 for cilia placement and ciliogenesis; nphp-2; nphp-4 double mutants are strongly synthetic (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3, warburtonpitt2015theciliopathygene pages 95-99) |
| Key genetic interactions: MKS/TZ module | Genetically interacts with mks-1, mks-3, mks-6, mksr-1, mksr-2 and other TZ-associated components in a sensillum-dependent manner (warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2, warburtonpitt2015theciliopathygene pages 104-108, warburtonpitt2015theciliopathygene pages 95-99) |
| Key genetic interactions: ARL-13/doublet-region module | Interacts with arl-13, klp-11, unc-119, with modules organized as nphp-2 + klp-11 and arl-13 + unc-119, antagonized by hdac-6; these modules regulate ciliary microtubule patterning and compartment size (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 1-2) |
| Ciliary signaling/protein localization roles | Required for localization of TAX-2 and partially for TAX-4 to the proximal cilium/InvC; also linked to compartmentalization of signaling proteins in cilia (warburtonpitt2015theciliopathygene pages 29-33, blacque2014compartmentswithina pages 7-8) |
| Mutant phenotypes | Dye-filling (Dyf) defects, transition zone/cilia displacement, mispositioned phasmid cilia, defective cilia orientation, and shorter phasmid dendrites; double mutants can show severe loss of cilia and major microtubule ultrastructural defects (warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4, warburtonpitt2012ciliogenesisincaenorhabditis pages 8-9, warburtonpitt2015theciliopathygene pages 95-99, warburtonpitt2014thenphp2and pages 4-5) |
| Microtubule/ultrastructure effects | Required for proper microtubule patterning, including alignment of doublet/singlet regions, Y-link organization, and regulation of tubulin glutamylation together with the ARL-13 module (warburtonpitt2014thenphp2and pages 2-3, warburtonpitt2014thenphp2and pages 1-2, warburtonpitt2014thenphp2and pages 4-5) |
| Subcompartment control | The MKS-5/RPGRIP1L-dependent transition zone/CIZE helps confine NPHP-2 and other signaling proteins to appropriate ciliary subdomains, supporting stable ciliary compartmentalization (jensen2015formationofthe pages 1-2, jensen2015formationofthe pages 12-14) |
Table: This table summarizes the verified identity, domains, localization, genetic interactions, and mutant phenotypes of the C. elegans ciliary protein NPHP-2/Y32G9A.6. It is useful as a compact reference for functional annotation and for distinguishing nphp-2 from other ankyrin-repeat proteins such as mlt-4.
NPHP-2 (Y32G9A.6) is the C. elegans ortholog of mammalian inversin/NPHP2, an ankyrin repeat and EF-hand domain-containing protein that functions as a ciliary structural organizer and genetic modifier rather than an enzyme or transporter. Its primary role is in the Inversin compartment (InvC) of sensory cilia, where it coordinates ciliogenesis, cilia placement and orientation, microtubule ultrastructural patterning, tubulin post-translational modifications, and ciliary protein compartmentalization. NPHP-2 acts as a physical and genetic nexus connecting the NPHP, MKS/transition zone, and doublet region protein modules. Its function requires calcium-sensing through its EF-hand domain and protein–protein interactions mediated by its ankyrin repeats. The protein serves as a valuable model for understanding ciliopathies, particularly nephronophthisis, and the molecular mechanisms underlying ciliary subcompartmentalization.
References
(OpenTargets Search: nephronophthisis-INVS): Open Targets Query (nephronophthisis-INVS, 14 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.
(warburtonpitt2012ciliogenesisincaenorhabditis pages 1-2): Simon R. F. Warburton-Pitt, Andrew R. Jauregui, Chunmei Li, Juan Wang, M. Leroux, and M. Barr. Ciliogenesis in caenorhabditis elegans requires genetic interactions between ciliary middle segment localized nphp-2 (inversin) and transition zone-associated proteins. Journal of Cell Science, 125:2592-2603, Jun 2012. URL: https://doi.org/10.1242/jcs.095539, doi:10.1242/jcs.095539. This article has 57 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2015theciliopathygene pages 108-114): Simon R. F. Warburton-Pitt. The ciliopathy gene nphp 2 functions in multiple gene networks and regulates ciliogenesis in c. elegans. ArXiv, Jan 2015. URL: https://doi.org/10.7282/t3v40wx3, doi:10.7282/t3v40wx3. This article has 0 citations.
(warburtonpitt2015theciliopathygene pages 104-108): Simon R. F. Warburton-Pitt. The ciliopathy gene nphp 2 functions in multiple gene networks and regulates ciliogenesis in c. elegans. ArXiv, Jan 2015. URL: https://doi.org/10.7282/t3v40wx3, doi:10.7282/t3v40wx3. This article has 0 citations.
(warburtonpitt2012ciliogenesisincaenorhabditis pages 3-4): Simon R. F. Warburton-Pitt, Andrew R. Jauregui, Chunmei Li, Juan Wang, M. Leroux, and M. Barr. Ciliogenesis in caenorhabditis elegans requires genetic interactions between ciliary middle segment localized nphp-2 (inversin) and transition zone-associated proteins. Journal of Cell Science, 125:2592-2603, Jun 2012. URL: https://doi.org/10.1242/jcs.095539, doi:10.1242/jcs.095539. This article has 57 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2015theciliopathygene pages 29-33): Simon R. F. Warburton-Pitt. The ciliopathy gene nphp 2 functions in multiple gene networks and regulates ciliogenesis in c. elegans. ArXiv, Jan 2015. URL: https://doi.org/10.7282/t3v40wx3, doi:10.7282/t3v40wx3. This article has 0 citations.
(warburtonpitt2014thenphp2and pages 4-5): Simon R. F. Warburton-Pitt, Malan Silva, Ken C. Q. Nguyen, David H. Hall, and Maureen M. Barr. The nphp-2 and arl-13 genetic modules interact to regulate ciliogenesis and ciliary microtubule patterning in c. elegans. PLoS Genetics, 10:e1004866, Dec 2014. URL: https://doi.org/10.1371/journal.pgen.1004866, doi:10.1371/journal.pgen.1004866. This article has 44 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2014thenphp2and pages 10-11): Simon R. F. Warburton-Pitt, Malan Silva, Ken C. Q. Nguyen, David H. Hall, and Maureen M. Barr. The nphp-2 and arl-13 genetic modules interact to regulate ciliogenesis and ciliary microtubule patterning in c. elegans. PLoS Genetics, 10:e1004866, Dec 2014. URL: https://doi.org/10.1371/journal.pgen.1004866, doi:10.1371/journal.pgen.1004866. This article has 44 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2012ciliogenesisincaenorhabditis pages 2-3): Simon R. F. Warburton-Pitt, Andrew R. Jauregui, Chunmei Li, Juan Wang, M. Leroux, and M. Barr. Ciliogenesis in caenorhabditis elegans requires genetic interactions between ciliary middle segment localized nphp-2 (inversin) and transition zone-associated proteins. Journal of Cell Science, 125:2592-2603, Jun 2012. URL: https://doi.org/10.1242/jcs.095539, doi:10.1242/jcs.095539. This article has 57 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2014thenphp2and pages 1-2): Simon R. F. Warburton-Pitt, Malan Silva, Ken C. Q. Nguyen, David H. Hall, and Maureen M. Barr. The nphp-2 and arl-13 genetic modules interact to regulate ciliogenesis and ciliary microtubule patterning in c. elegans. PLoS Genetics, 10:e1004866, Dec 2014. URL: https://doi.org/10.1371/journal.pgen.1004866, doi:10.1371/journal.pgen.1004866. This article has 44 citations and is from a domain leading peer-reviewed journal.
(jensen2015formationofthe pages 1-2): Victor L Jensen, Chunmei Li, Rachel V Bowie, Lara Clarke, Swetha Mohan, Oliver E Blacque, and Michel R Leroux. Formation of the transition zone by mks5/rpgrip1l establishes a ciliary zone of exclusion (cize) that compartmentalises ciliary signalling proteins and controls pip2 ciliary abundance. The EMBO Journal, 34:2537-2556, Oct 2015. URL: https://doi.org/10.15252/embj.201488044, doi:10.15252/embj.201488044. This article has 164 citations.
(jensen2015formationofthe pages 12-14): Victor L Jensen, Chunmei Li, Rachel V Bowie, Lara Clarke, Swetha Mohan, Oliver E Blacque, and Michel R Leroux. Formation of the transition zone by mks5/rpgrip1l establishes a ciliary zone of exclusion (cize) that compartmentalises ciliary signalling proteins and controls pip2 ciliary abundance. The EMBO Journal, 34:2537-2556, Oct 2015. URL: https://doi.org/10.15252/embj.201488044, doi:10.15252/embj.201488044. This article has 164 citations.
(warburtonpitt2012ciliogenesisincaenorhabditis pages 7-8): Simon R. F. Warburton-Pitt, Andrew R. Jauregui, Chunmei Li, Juan Wang, M. Leroux, and M. Barr. Ciliogenesis in caenorhabditis elegans requires genetic interactions between ciliary middle segment localized nphp-2 (inversin) and transition zone-associated proteins. Journal of Cell Science, 125:2592-2603, Jun 2012. URL: https://doi.org/10.1242/jcs.095539, doi:10.1242/jcs.095539. This article has 57 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2015theciliopathygene pages 95-99): Simon R. F. Warburton-Pitt. The ciliopathy gene nphp 2 functions in multiple gene networks and regulates ciliogenesis in c. elegans. ArXiv, Jan 2015. URL: https://doi.org/10.7282/t3v40wx3, doi:10.7282/t3v40wx3. This article has 0 citations.
(warburtonpitt2012ciliogenesisincaenorhabditis pages 8-9): Simon R. F. Warburton-Pitt, Andrew R. Jauregui, Chunmei Li, Juan Wang, M. Leroux, and M. Barr. Ciliogenesis in caenorhabditis elegans requires genetic interactions between ciliary middle segment localized nphp-2 (inversin) and transition zone-associated proteins. Journal of Cell Science, 125:2592-2603, Jun 2012. URL: https://doi.org/10.1242/jcs.095539, doi:10.1242/jcs.095539. This article has 57 citations and is from a domain leading peer-reviewed journal.
(warburtonpitt2014thenphp2and pages 2-3): Simon R. F. Warburton-Pitt, Malan Silva, Ken C. Q. Nguyen, David H. Hall, and Maureen M. Barr. The nphp-2 and arl-13 genetic modules interact to regulate ciliogenesis and ciliary microtubule patterning in c. elegans. PLoS Genetics, 10:e1004866, Dec 2014. URL: https://doi.org/10.1371/journal.pgen.1004866, doi:10.1371/journal.pgen.1004866. This article has 44 citations and is from a domain leading peer-reviewed journal.
(blacque2014compartmentswithina pages 7-8): Oliver E Blacque and Anna AWM Sanders. Compartments within a compartment. Organogenesis, 10:126-137, Jan 2014. URL: https://doi.org/10.4161/org.28830, doi:10.4161/org.28830. This article has 75 citations.
(cevik2013activetransportand pages 5-6): Sebiha Cevik, Anna A. W. M. Sanders, Erwin Van Wijk, Karsten Boldt, Lara Clarke, Jeroen van Reeuwijk, Yuji Hori, Nicola Horn, Lisette Hetterschijt, Anita Wdowicz, Andrea Mullins, Katarzyna Kida, Oktay I. Kaplan, Sylvia E. C. van Beersum, Ka Man Wu, Stef J. F. Letteboer, Dorus A. Mans, Toshiaki Katada, Kenji Kontani, Marius Ueffing, Ronald Roepman, Hannie Kremer, and Oliver E. Blacque. Active transport and diffusion barriers restrict joubert syndrome-associated arl13b/arl-13 to an inv-like ciliary membrane subdomain. PLoS Genetics, 9:e1003977, Dec 2013. URL: https://doi.org/10.1371/journal.pgen.1003977, doi:10.1371/journal.pgen.1003977. This article has 115 citations and is from a domain leading peer-reviewed journal.
(beyrent2024dimerizationactivatesthe pages 1-2): Erika Beyrent, Derek T. Wei, Gwendolyn M. Beacham, Sangwoo Park, Jian Zheng, Matthew J. Paszek, and Gunther Hollopeter. Dimerization activates the inversin complex in c. elegans. Molecular Biology of the Cell, Oct 2024. URL: https://doi.org/10.1091/mbc.e24-05-0218, doi:10.1091/mbc.e24-05-0218. This article has 5 citations and is from a domain leading peer-reviewed journal.
(veland2013inversinnephrocystin2isrequired pages 4-4): Iben R. Veland, Rodrick Montjean, Lorraine Eley, Lotte B. Pedersen, Albrecht Schwab, Judith Goodship, Karsten Kristiansen, Stine F. Pedersen, Sophie Saunier, and Søren T. Christensen. Inversin/nephrocystin-2 is required for fibroblast polarity and directional cell migration. PLoS ONE, 8:e60193, Apr 2013. URL: https://doi.org/10.1371/journal.pone.0060193, doi:10.1371/journal.pone.0060193. This article has 86 citations and is from a peer-reviewed journal.
(goggolidou2014wntandplanar pages 2-4): Paraskevi Goggolidou. Wnt and planar cell polarity signaling in cystic renal disease. Organogenesis, 10:86-95, Oct 2014. URL: https://doi.org/10.4161/org.26766, doi:10.4161/org.26766. This article has 80 citations.
(veland2013inversinnephrocystin2isrequired pages 1-2): Iben R. Veland, Rodrick Montjean, Lorraine Eley, Lotte B. Pedersen, Albrecht Schwab, Judith Goodship, Karsten Kristiansen, Stine F. Pedersen, Sophie Saunier, and Søren T. Christensen. Inversin/nephrocystin-2 is required for fibroblast polarity and directional cell migration. PLoS ONE, 8:e60193, Apr 2013. URL: https://doi.org/10.1371/journal.pone.0060193, doi:10.1371/journal.pone.0060193. This article has 86 citations and is from a peer-reviewed journal.
(veland2013inversinnephrocystin2isrequired pages 12-13): Iben R. Veland, Rodrick Montjean, Lorraine Eley, Lotte B. Pedersen, Albrecht Schwab, Judith Goodship, Karsten Kristiansen, Stine F. Pedersen, Sophie Saunier, and Søren T. Christensen. Inversin/nephrocystin-2 is required for fibroblast polarity and directional cell migration. PLoS ONE, 8:e60193, Apr 2013. URL: https://doi.org/10.1371/journal.pone.0060193, doi:10.1371/journal.pone.0060193. This article has 86 citations and is from a peer-reviewed journal.
(warburtonpitt2015theciliopathygene pages 40-44): Simon R. F. Warburton-Pitt. The ciliopathy gene nphp 2 functions in multiple gene networks and regulates ciliogenesis in c. elegans. ArXiv, Jan 2015. URL: https://doi.org/10.7282/t3v40wx3, doi:10.7282/t3v40wx3. This article has 0 citations.