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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
car-1 encodes a conserved LSM14/Scd6/Rap55-family RNA-binding protein that partitions into cytoplasmic ribonucleoprotein (RNP) condensates (P-bodies/P-body-like foci and germ granules) and coordinates post-transcriptional control of specific mRNAs. Rather than catalyzing a biochemical reaction, CAR-1 acts as an adaptor/scaffold that (i) promotes translational repression and mRNP granule association, (ii) interfaces with mRNA decapping/decay factors in a context-dependent manner, and (iii) couples RNA regulation to membrane/ER organization and developmental programs including embryonic cytokinesis, oogenesis, neuronal axon regeneration, and germline small-RNA inheritance. Foundational cell-biological evidence established CAR-1 colocalization with the decapping cofactor DCAP-1 and requirements for cytokinesis and ER organization in embryos, while recent work (2023–2024) positions CAR-1 as a key organizer at the P-body–germ-granule interface in piRNA-dependent transgenerational silencing and as a regulated target/participant of embryonic mRNA clearance pathways that specialize decapping condensates. (squirrell2006car1aprotein pages 1-2, decker2006car1andtrailer pages 3-4, du2023condensatecooperativityunderlies pages 5-6, vidya2024edc3andedc4 pages 9-12, vidya2024edc3andedc4 pages 5-9)
Multiple independent sources explicitly match the requested target: C. elegans CAR-1 is a member of the LSM14/Scd6/Rap55 family of Sm-like RNA-binding proteins. Squirrell et al. reported a predicted ~340-aa glycine-rich protein with clustered RGG motifs (RGG box) and clear homologs (Xenopus RAP55, yeast Scd6p/Lsm13p, Drosophila Trailer Hitch), consistent with UniProt Q9XW17 family assignment. (squirrell2006car1aprotein pages 1-2) Decker & Parker classified CAR-1 as the C. elegans Scd6 ortholog, noting an N-terminal Lsm domain (family feature) and poly(U) binding by the RGG region. (decker2006car1andtrailer pages 2-3, decker2006car1andtrailer pages 1-2) Later work explicitly referred to CAR-1 as CAR-1/LSM14. (tang2020themrnadecay pages 1-3, vidya2024edc3andedc4 pages 1-5)
LSM14-family proteins are conserved RNA-associated factors enriched in cytoplasmic mRNP granules. Mechanistically, they are frequently discussed as components of translation repression complexes and P-bodies, with conserved low-complexity/RGG regions enabling RNA binding and assembly into higher-order RNPs. (decker2006car1andtrailer pages 2-3, decker2006car1andtrailer pages 1-2)
P-bodies are cytoplasmic condensates enriched in translationally repressed mRNAs and factors for mRNA turnover (decapping and 5′→3′ decay). A key expert framing is that P-bodies can act as sites where mRNAs are held in a repressed state and later returned to translation or routed to decay, and that granule aggregation may support mRNA transport and maintenance of translational repression. (decker2006car1andtrailer pages 1-2, decker2006car1andtrailer pages 4-4)
In C. elegans, CAR-1 localizes both to P granules (germ granules) and to DCAP-1-positive cytoplasmic foci interpreted as P-body-like structures. (squirrell2006car1aprotein pages 6-7)
Recent C. elegans work emphasizes that multiple condensate types (P-bodies, germ granules, stress granules) can coexist and interact, and that developmentally regulated clearance of mRNAs encoding condensate scaffolds helps shape condensate composition across embryogenesis. (vidya2024edc3andedc4 pages 1-5, vidya2024edc3andedc4 pages 19-23)
CAR-1 is not an enzyme; it is best annotated as an RNA-binding mRNP assembly/adaptor protein that promotes translational repression and can channel mRNAs toward, or away from, decapping/decay depending on developmental context.
Direct/functional evidence for RNA-binding and repression: CAR-1’s RGG region binds poly(U) in vitro, supporting direct RNA-binding capacity. (decker2006car1andtrailer pages 1-2) In the germline/oogenesis, CAR-1 promotes PUF-dependent repression of the Notch-like receptor mRNA glp-1, and car-1 depletion elevates GLP-1 protein while glp-1 mRNA levels remain similar, consistent with primary control at the translation level. (noble2008maternalmrnasare pages 8-9)
Context-dependent relationship to decapping/decay: CAR-1 colocalizes with decapping machinery and can be described as an mRNA decay-associated factor in neurons; in other settings CAR-1 participates in complexes that repress translation and can prevent decapping/decay. (tang2020themrnadecay pages 3-4, vidya2024edc3andedc4 pages 1-5)
CAR-1 localizes broadly in cytoplasm but concentrates in at least two granule populations: (i) PGL-1-positive P granules and (ii) smaller DCAP-1-positive cytoplasmic foci; figure evidence from Squirrell et al. captures CAR-1 colocalization with both PGL-1 and DCAP-1. (squirrell2006car1aprotein pages 6-7, squirrell2006car1aprotein media 35d21d13)
CAR-1 is also functionally coupled to the endoplasmic reticulum (ER) in embryos, where depletion disrupts ER reticulation and spindle/midzone-associated ER, consistent with an ER-linked mRNP/granule function. (decker2006car1andtrailer pages 3-4)
In neurons, CAR-1 forms cytoplasmic puncta in cell bodies that fully colocalize with CGH-1/DDX6 and partially with DCAP-1, suggesting heterogeneous CAR-1 granules with variable decapping factor content. (tang2020themrnadecay pages 3-4)
Embryogenesis: cytokinesis and ER organization. CAR-1 is required for late cytokinesis/scission; depletion causes cleavage furrows to ingress then regress and disrupts membrane accumulation and spindle midzone organization, accompanied by ER morphology defects. (squirrell2006car1aprotein pages 1-2, decker2006car1andtrailer pages 3-4, squirrell2006car1aprotein media cc00f993)
Germline/oogenesis: maternal mRNA control. CAR-1 contributes to stage-specific translational repression of maternal mRNAs, including glp-1, and genetically interacts with PUF proteins, supporting a model where CAR-1 acts with sequence-specific RBPs to enforce developmental timing of translation. (noble2008maternalmrnasare pages 7-8, noble2008maternalmrnasare pages 8-9)
Neurons: axon regeneration via mitochondrial Ca2+ regulation. Tang et al. describe CAR-1/LSM14 as a translational repressor/mRNA decay factor that represses neuronal micu-1, thereby modulating mitochondrial Ca2+ uptake dynamics after axotomy and acting as a cell-intrinsic inhibitor of PLM axon regrowth. (tang2020themrnadecay pages 1-3, tang2020themrnadecay pages 3-4)
Germline inheritance: piRNA-dependent transgenerational silencing. Du et al. (2023) identify CAR-1 as a P-body component required for proper CGH-1/DDX6 perinuclear condensates and for robust interaction of CGH-1 with piRNA pathway factors (e.g., PRG-1, WAGO-1); car-1 RNAi disperses CGH-1 and reduces these interactions, impairing piRNA reporter silencing readouts. (du2023condensatecooperativityunderlies pages 5-6, du2023condensatecooperativityunderlies pages 24-29)
A central 2023 advance is that CAR-1 is implicated in organizing condensate–condensate interactions at the cytoplasmic face of perinuclear germ granules: CAR-1 promotes CGH-1 perinuclear localization/condensate formation, and CAR-1 depletion reduces CGH-1 binding to PRG-1 and WAGO-1 and perturbs perinuclear localization of PRG-1/WAGO-4, linking CAR-1 to piRNA pathway architecture. (du2023condensatecooperativityunderlies pages 5-6, du2023condensatecooperativityunderlies pages 24-29)
Vidya et al. (bioRxiv, 2024-03-04) report that decapping scaffolds EDC-3 and EDC-4 shape DCAP-2 condensates in embryos and promote timed clearance of mRNAs including car-1. (vidya2024edc3andedc4 pages 1-5, vidya2024edc3andedc4 pages 19-23)
Quantitatively, the authors show the DCAP-2 interactome changes markedly in edc-3(0);edc-4(0) embryos, with increased association to IFET-1, CAR-1, and CGH-1, and that car-1 RNAi (64% knockdown) in this background reduces DCAP-2 foci 2–4.5-fold, supporting a scaffold role for CAR-1 in alternative condensate frameworks when canonical scaffolds are absent. (vidya2024edc3andedc4 pages 9-12)
Elaswad et al. (MBoC, 2024-10) identify CCT chaperonin and actin as inhibitors of ectopic RNA-binding protein condensation during oogenesis and connect ER sheet expansion to induction of condensates containing CAR-1. (elaswad2024thecctchaperonin pages 1-2, elaswad2024thecctchaperonin pages 11-13) They further link ectopic condensation of regulators including CAR-1 to translational derepression of a maternal mRNA readout (spn-4), with quantitative imaging of SPN-4::GFP increases upon cct-2 depletion. (elaswad2024thecctchaperonin pages 10-11)
CAR-1’s robust granule localization across germline, embryo, and neurons makes it a practical marker and perturbation target to study: (i) condensate material properties and stress responses, (ii) coupling between RNA regulation and organelle organization (ER), and (iii) inter-condensate organization supporting small-RNA inheritance. Imaging work operationalized CAR-1 “condensation” by cortex granule counts, showing time-dependent increases under imaging stress (40% condensed at 11–20 min; 60–100% after >30 min), highlighting methodological implications for live imaging of condensates. (elaswad2022imagingassociatedstresscauses pages 7-8)
The CAR-1 family is conserved (LSM14A/LSM14B in mammals), and expert framing posits Scd6/LSM14 proteins as conserved integrators of translational repression and mRNA storage/decay in P-bodies, sometimes associated with ER-linked local translation. (decker2006car1andtrailer pages 1-2, decker2006car1andtrailer pages 4-4)
In disease-relevant cell biology, a 2024 Nature Cell Biology paper isolated LSM14A-GFP+ P-bodies from leukemia cell lysates by particle sorting and performed RNA-seq, providing a real-world example where LSM14-family proteins enable biochemical purification of P-bodies to define disease-associated RNA sequestration programs. (squirrell2006car1aprotein media 35d21d13)
A widely cited expert perspective is that aggregation of mRNPs into granules can facilitate mRNA transport and help maintain translational repression, and that P-bodies are dynamic sites where mRNAs can be stored for reactivation or routed to decay. This conceptual framework supports interpreting CAR-1 phenotypes (translation control, developmental timing, and context-dependent links to decapping) through a granule-centric model rather than a single linear decay pathway. (decker2006car1andtrailer pages 1-2)
Key quantitative findings supporting functional annotation include:
| Aspect | Key findings (1-3 bullets) | Evidence | URL/DOI | Pub date |
|---|---|---|---|---|
| identity/domains | • car-1 in C. elegans encodes an LSM14/Rap55/Scd6-family Sm-like RNA-binding protein. • Protein features reported in primary literature include a glycine-rich C-terminus with clustered RGG motifs/RGG box; review literature notes N-terminal Lsm domain and RNA binding/poly(U) binding, consistent with UniProt family/domain assignment. • Homology links CAR-1 to RAP55, Trailer Hitch, Scd6 family proteins. |
Squirrell 2006 showed CAR-1 is a predicted 340-aa protein with clustered RGG motifs and homologs including RAP55, Scd6p/Lsm13p and Trailer Hitch; Decker & Parker 2006 classified CAR-1 as a Scd6-family/Lsm protein with RNA-binding properties; Tang 2020 explicitly identified CAR-1 as CAR-1/LSM14; Vidya 2024 listed CAR-1 as LSm14 (squirrell2006car1aprotein pages 1-2, decker2006car1andtrailer pages 2-3, tang2020themrnadecay pages 1-3, vidya2024edc3andedc4 pages 1-5). | https://doi.org/10.1091/mbc.e05-09-0874; https://doi.org/10.1083/jcb.200601153; https://doi.org/10.1016/j.cub.2019.12.061; https://doi.org/10.1101/2024.03.04.583404 | Jan 2006; Apr 2006; Mar 2020; Mar 2024 |
| molecular function | • Functions primarily as an RNA-associated translational repressor / mRNP assembly factor rather than an enzyme. • Acts with CGH-1/DDX6 and can interface with mRNA decapping machinery (DCAP-1/DCAP-2), with context-dependent roles in either repressing translation and protecting mRNAs or promoting entry into decay pathways. • Regulates specific targets, including glp-1 mRNA in oogenesis and micu-1 in neurons. |
Noble 2008 showed CAR-1 promotes repression of glp-1 during late oogenesis and that glp-1 mRNA levels can remain unchanged while GLP-1 protein rises after car-1 perturbation, supporting translational control; Tang 2020 showed CAR-1 binds mature mRNAs with CGH-1, colocalizes with decapping factors, and represses neuronal micu-1; Vidya 2024 reported CAR-1/CGH-1/IFET-1 complexes can repress translation and prevent decapping/decay in some developmental contexts while CAR-1 is also linked to higher-order decapping assemblies (noble2008maternalmrnasare pages 7-8, noble2008maternalmrnasare pages 8-9, tang2020themrnadecay pages 3-4, vidya2024edc3andedc4 pages 1-5). | https://doi.org/10.1083/jcb.200802128; https://doi.org/10.1016/j.cub.2019.12.061; https://doi.org/10.1101/2024.03.04.583404 | Aug 2008; Mar 2020; Mar 2024 |
| localization | • Localizes to cytoplasmic RNA granules, including P-granules/germ granules and smaller DCAP-1-positive cytoplasmic foci/P-body-like granules. • Has functional/physical links to the ER in embryos; neuronal CAR-1 forms cytoplasmic puncta with CGH-1 and partly with DCAP-1. • Recent imaging work supports CAR-1 as a regulated condensate component whose condensation increases under stress or oocyte arrest. |
Squirrell 2006 showed GFP::CAR-1 colocalizes with PGL-1 in P-granules and with DCAP-1 in cytoplasmic foci, and linked CAR-1 depletion to ER disorganization; figure evidence confirms CAR-1/DCAP-1 foci and ER defects (squirrell2006car1aprotein pages 6-7, squirrell2006car1aprotein media 35d21d13). Tang 2020 found neuronal CAR-1 puncta fully colocalize with CGH-1 and partially with DCAP-1 (tang2020themrnadecay pages 3-4, tang2020themrnadecay pages 1-3). Elaswad 2022 quantified stress-induced CAR-1 condensation in germline/oocyte contexts (elaswad2022imagingassociatedstresscauses pages 7-8). | https://doi.org/10.1091/mbc.e05-09-0874; https://doi.org/10.1016/j.cub.2019.12.061; https://doi.org/10.1093/g3journal/jkac172 | Jan 2006; Mar 2020; Jul 2022 |
| biological processes | • Required for late cytokinesis and normal ER organization in embryos. • Contributes to maternal mRNA regulation/oogenesis, including repression of glp-1 and proper oocyte/embryo development. • Also functions in axon regeneration control via mitochondrial calcium regulation and in piRNA/transgenerational gene silencing through condensate organization. |
Squirrell 2006 showed car-1 loss causes furrow regression, absent spindle midzone, and ER defects in embryos (squirrell2006car1aprotein pages 1-2, decker2006car1andtrailer pages 3-4). Noble 2008 linked CAR-1 to late-oogenesis repression of glp-1 and strong genetic interactions with puf-5 affecting oogenesis/embryogenesis (noble2008maternalmrnasare pages 7-8, noble2008maternalmrnasare pages 8-9). Tang 2020 identified CAR-1 as a cell-intrinsic inhibitor of axon regrowth through repression of micu-1 and modulation of mitochondrial Ca2+ dynamics (tang2020themrnadecay pages 3-4, tang2020themrnadecay pages 1-3). Du 2023 showed CAR-1 promotes CGH-1 interactions with piRNA factors and supports transgenerational silencing-related condensate organization (du2023condensatecooperativityunderlies pages 5-6, du2023condensatecooperativityunderlies pages 24-29). | https://doi.org/10.1091/mbc.e05-09-0874; https://doi.org/10.1083/jcb.200802128; https://doi.org/10.1016/j.cub.2019.12.061; https://doi.org/10.1016/j.celrep.2023.112859 | Jan 2006; Aug 2008; Mar 2020; Aug 2023 |
| recent developments 2023-2024 | • 2023: CAR-1 emerged as a key P-body factor organizing interactions between P-bodies and perinuclear germ granules to support piRNA-dependent transgenerational silencing. • 2024: CAR-1 was implicated in embryonic mRNA clearance / P-body specialization via interactions with EDC-3/EDC-4 and the IFET-1/CAR-1/CGH-1 complex. • 2024: Oogenesis work connected CAR-1 condensation to ER morphology, CCT/actin, and maintenance of translational repression/oocyte quality. |
Du 2023 showed car-1 RNAi disperses CGH-1 from perinuclear P bodies, reduces CGH-1 interactions with PRG-1/WAGO-1, and impairs piRNA reporter silencing (du2023condensatecooperativityunderlies pages 5-6, du2023condensatecooperativityunderlies pages 24-29). Vidya 2024 showed EDC-3 promotes clearance of car-1 mRNA and that CAR-1 helps scaffold DCAP-2 condensates when EDC-3/EDC-4 are absent (vidya2024edc3andedc4 pages 9-12, vidya2024edc3andedc4 pages 16-19, vidya2024edc3andedc4 pages 1-5). Elaswad 2024 linked CAR-1 ectopic condensation to CCT/actin depletion and expanded ER sheets during oogenesis (elaswad2024thecctchaperonin pages 11-13, elaswad2024thecctchaperonin pages 7-8, elaswad2024thecctchaperonin pages 1-2). | https://doi.org/10.1016/j.celrep.2023.112859; https://doi.org/10.1101/2024.03.04.583404; https://doi.org/10.1091/mbc.e24-05-0216 | Aug 2023; Mar 2024; Oct 2024 |
| quantitative stats/data | • Axon regeneration: car-1(0) increased PLM axon regrowth/growth-cone formation; analyses used n ≳100, with p < 0.01 to p < 0.001 depending on comparison. • Oogenesis/embryogenesis: in car-1; puf-5 perturbation, phenotype penetrance was high: small oocytes 86% (n=36), yolk accumulation 84% (n=37), eggshell defects 90% (n=49), cytokinesis defects 98% (n=203). • Recent datasets: car-1 RNAi reduced DCAP-2 foci 2- to 4.5-fold in edc-3(0);edc-4(0) embryos; car-1/car-1 mRNA increased ~1.4-fold in edc-3(0) and ~1.6-fold in edc-3(0);edc-4(0); imaging stress induced CAR-1 condensation in 40% of worms at 11-20 min and 60-100% after >30 min; CAR-1 K185R extended lifespan to 22.51 ± 0.60 d vs 14.70 ± 0.59 d WT and car-1 loss shortened lifespan to 14.81 ± 0.41 d vs 17.56 ± 0.52 d WT. |
Tang 2020 reported significant regeneration phenotypes with Fisher’s exact test / ANOVA and large sample sizes (tang2020themrnadecay pages 3-4). Noble 2008 provided penetrance/sample-size values for combined car-1/puf-5 phenotypes (noble2008maternalmrnasare pages 7-8). Vidya 2024 quantified CAR-1-dependent DCAP-2 foci reduction and car-1 mRNA increases in edc mutants (vidya2024edc3andedc4 pages 9-12, vidya2024edc3andedc4 pages 16-19). Elaswad 2022 quantified stress-induced CAR-1 condensation frequencies (elaswad2022imagingassociatedstresscauses pages 7-8). Moll 2018 quantified lifespan and SUMOylation-linked CAR-1 effects (moll2018theinsulinigfsignaling pages 6-8, moll2018theinsulinigfsignaling pages 3-6). | https://doi.org/10.1016/j.cub.2019.12.061; https://doi.org/10.1083/jcb.200802128; https://doi.org/10.1101/2024.03.04.583404; https://doi.org/10.1093/g3journal/jkac172; https://doi.org/10.7554/eLife.38635 | Mar 2020; Aug 2008; Mar 2024; Jul 2022; Nov 2018 |
Table: This table summarizes evidence-based functional annotation for C. elegans car-1/LSM14 (UniProt Q9XW17), covering identity, molecular function, localization, biology, recent 2023-2024 developments, and quantitative findings. It is limited to claims directly supported by the provided context IDs.
Despite targeted retrieval, directly accessible 2023–2024 review articles focusing specifically on C. elegans CAR-1 (as opposed to broader condensate/P-body reviews) were limited in the acquired corpus; therefore, expert commentary is primarily drawn from a classic mini-review (2006) and integrated with 2023–2024 primary studies. Claims in this report are restricted to those supported by the cited evidence.
References
(squirrell2006car1aprotein pages 1-2): Jayne M. Squirrell, Zachary T. Eggers, Nancy Luedke, Bonnie Saari, Andrew Grimson, Gary E. Lyons, Philip Anderson, and John G. White. Car-1, a protein that localizes with the mrna decapping component dcap-1, is required for cytokinesis and er organization incaenorhabditis elegansembryos. Jan 2006. URL: https://doi.org/10.1091/mbc.e05-09-0874, doi:10.1091/mbc.e05-09-0874. This article has 104 citations and is from a domain leading peer-reviewed journal.
(decker2006car1andtrailer pages 3-4): Carolyn J. Decker and Roy Parker. Car-1 and trailer hitch: driving mrnp granule function at the er? The Journal of Cell Biology, 173:159-163, Apr 2006. URL: https://doi.org/10.1083/jcb.200601153, doi:10.1083/jcb.200601153. This article has 52 citations.
(du2023condensatecooperativityunderlies pages 5-6): Zhenzhen Du, Kun Shi, Jordan S. Brown, Tao He, Wei-Sheng Wu, Ying Zhang, Heng-Chi Lee, and Donglei Zhang. Condensate cooperativity underlies transgenerational gene silencing. Cell Reports, 42:112859, Aug 2023. URL: https://doi.org/10.1016/j.celrep.2023.112859, doi:10.1016/j.celrep.2023.112859. This article has 27 citations and is from a highest quality peer-reviewed journal.
(vidya2024edc3andedc4 pages 9-12): Elva Vidya, Yasaman Jami-Alahmadi, Adarsh K. Mayank, Javeria Rizwan, Jia Ming Stella Xu, Tianhao Cheng, Rania Leventis, Nahum Sonenberg, James A. Wohlschlegel, Maria Vera, and Thomas F. Duchaine. Edc-3 and edc-4 regulate embryonic mrna clearance and biomolecular condensate specialization. bioRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.04.583404, doi:10.1101/2024.03.04.583404. This article has 8 citations.
(vidya2024edc3andedc4 pages 5-9): Elva Vidya, Yasaman Jami-Alahmadi, Adarsh K. Mayank, Javeria Rizwan, Jia Ming Stella Xu, Tianhao Cheng, Rania Leventis, Nahum Sonenberg, James A. Wohlschlegel, Maria Vera, and Thomas F. Duchaine. Edc-3 and edc-4 regulate embryonic mrna clearance and biomolecular condensate specialization. bioRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.04.583404, doi:10.1101/2024.03.04.583404. This article has 8 citations.
(decker2006car1andtrailer pages 2-3): Carolyn J. Decker and Roy Parker. Car-1 and trailer hitch: driving mrnp granule function at the er? The Journal of Cell Biology, 173:159-163, Apr 2006. URL: https://doi.org/10.1083/jcb.200601153, doi:10.1083/jcb.200601153. This article has 52 citations.
(decker2006car1andtrailer pages 1-2): Carolyn J. Decker and Roy Parker. Car-1 and trailer hitch: driving mrnp granule function at the er? The Journal of Cell Biology, 173:159-163, Apr 2006. URL: https://doi.org/10.1083/jcb.200601153, doi:10.1083/jcb.200601153. This article has 52 citations.
(tang2020themrnadecay pages 1-3): Ngang Heok Tang, Kyung Won Kim, Suhong Xu, Stephen M. Blazie, Brian A. Yee, Gene W. Yeo, Yishi Jin, and Andrew D. Chisholm. The mrna decay factor car-1/lsm14 regulates axon regeneration via mitochondrial calcium dynamics. Current Biology, 30:865-876.e7, Mar 2020. URL: https://doi.org/10.1016/j.cub.2019.12.061, doi:10.1016/j.cub.2019.12.061. This article has 34 citations and is from a highest quality peer-reviewed journal.
(vidya2024edc3andedc4 pages 1-5): Elva Vidya, Yasaman Jami-Alahmadi, Adarsh K. Mayank, Javeria Rizwan, Jia Ming Stella Xu, Tianhao Cheng, Rania Leventis, Nahum Sonenberg, James A. Wohlschlegel, Maria Vera, and Thomas F. Duchaine. Edc-3 and edc-4 regulate embryonic mrna clearance and biomolecular condensate specialization. bioRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.04.583404, doi:10.1101/2024.03.04.583404. This article has 8 citations.
(decker2006car1andtrailer pages 4-4): Carolyn J. Decker and Roy Parker. Car-1 and trailer hitch: driving mrnp granule function at the er? The Journal of Cell Biology, 173:159-163, Apr 2006. URL: https://doi.org/10.1083/jcb.200601153, doi:10.1083/jcb.200601153. This article has 52 citations.
(squirrell2006car1aprotein pages 6-7): Jayne M. Squirrell, Zachary T. Eggers, Nancy Luedke, Bonnie Saari, Andrew Grimson, Gary E. Lyons, Philip Anderson, and John G. White. Car-1, a protein that localizes with the mrna decapping component dcap-1, is required for cytokinesis and er organization incaenorhabditis elegansembryos. Jan 2006. URL: https://doi.org/10.1091/mbc.e05-09-0874, doi:10.1091/mbc.e05-09-0874. This article has 104 citations and is from a domain leading peer-reviewed journal.
(vidya2024edc3andedc4 pages 19-23): Elva Vidya, Yasaman Jami-Alahmadi, Adarsh K. Mayank, Javeria Rizwan, Jia Ming Stella Xu, Tianhao Cheng, Rania Leventis, Nahum Sonenberg, James A. Wohlschlegel, Maria Vera, and Thomas F. Duchaine. Edc-3 and edc-4 regulate embryonic mrna clearance and biomolecular condensate specialization. bioRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.04.583404, doi:10.1101/2024.03.04.583404. This article has 8 citations.
(noble2008maternalmrnasare pages 8-9): Scott L. Noble, Brittany L. Allen, Lai Kuan Goh, Kristen Nordick, and Thomas C. Evans. Maternal mrnas are regulated by diverse p body–related mrnp granules during early caenorhabditis elegans development. The Journal of Cell Biology, 182:559-572, Aug 2008. URL: https://doi.org/10.1083/jcb.200802128, doi:10.1083/jcb.200802128. This article has 148 citations.
(tang2020themrnadecay pages 3-4): Ngang Heok Tang, Kyung Won Kim, Suhong Xu, Stephen M. Blazie, Brian A. Yee, Gene W. Yeo, Yishi Jin, and Andrew D. Chisholm. The mrna decay factor car-1/lsm14 regulates axon regeneration via mitochondrial calcium dynamics. Current Biology, 30:865-876.e7, Mar 2020. URL: https://doi.org/10.1016/j.cub.2019.12.061, doi:10.1016/j.cub.2019.12.061. This article has 34 citations and is from a highest quality peer-reviewed journal.
(squirrell2006car1aprotein media 35d21d13): Jayne M. Squirrell, Zachary T. Eggers, Nancy Luedke, Bonnie Saari, Andrew Grimson, Gary E. Lyons, Philip Anderson, and John G. White. Car-1, a protein that localizes with the mrna decapping component dcap-1, is required for cytokinesis and er organization incaenorhabditis elegansembryos. Jan 2006. URL: https://doi.org/10.1091/mbc.e05-09-0874, doi:10.1091/mbc.e05-09-0874. This article has 104 citations and is from a domain leading peer-reviewed journal.
(squirrell2006car1aprotein media cc00f993): Jayne M. Squirrell, Zachary T. Eggers, Nancy Luedke, Bonnie Saari, Andrew Grimson, Gary E. Lyons, Philip Anderson, and John G. White. Car-1, a protein that localizes with the mrna decapping component dcap-1, is required for cytokinesis and er organization incaenorhabditis elegansembryos. Jan 2006. URL: https://doi.org/10.1091/mbc.e05-09-0874, doi:10.1091/mbc.e05-09-0874. This article has 104 citations and is from a domain leading peer-reviewed journal.
(noble2008maternalmrnasare pages 7-8): Scott L. Noble, Brittany L. Allen, Lai Kuan Goh, Kristen Nordick, and Thomas C. Evans. Maternal mrnas are regulated by diverse p body–related mrnp granules during early caenorhabditis elegans development. The Journal of Cell Biology, 182:559-572, Aug 2008. URL: https://doi.org/10.1083/jcb.200802128, doi:10.1083/jcb.200802128. This article has 148 citations.
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