| Annotated protein: | Adapter molecule crk (Proto-oncogene c-Crk) (p38). Gene symbol: CRK. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q64010 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ CRK |
| Ontology domain: | Biological Process |
| SynGO term: | postsynaptic specialization assembly (GO:0098698) |
| Synapse type(s): | Neuro-muscular junction |
| Annotated paper: | Hallock PT, et al. "Dok-7 regulates neuromuscular synapse formation by recruiting Crk and Crk-L" Genes Dev. 2010 Nov 1;24(21):2451-61 PMID:21041412 |
| Figure(s): | fig 7, fig 8 |
| Annotation description: | Crk-L is a postsynaptic protein which plays a crucial role in NMJ synapse formation concomitantly with CrkI/II, by directly interacting with Dok-7. Knockdown of both CrkI/II and Crk-L was necessary to induce a significant effect in postsynaptic AChR cluster formation, an effect that was partially rescued by overexpression of CrkL (Hallock et al., 2015). Transgenic mice lacking CrkL and CrkI/II in myotubes show neonatal lethality and study of their embryonic neuromuscular synapses reveal a lower number of synapses which resulted in a low level of innervated myofibers, decreased synaptic size and decreased number of synaptic AChRs. Moreover, motor axons grow beyond AChR cluster. Overall, CrkL has a crucial role in neuromuscular pre- and postsynaptic differentiation and its absence can be compensated by CrkI/II. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Confocal |
| Annotator(s): | Maria Andres-Alonso (ORCID:0000-0002-1585-539X) Michael Kreutz (ORCID:0000-0003-0575-6950) |
| Lab: | RG Neuroplasticity, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany and Leibniz Group 'Dendritic Organelles and Synaptic Function', Center for Molecular Neurobiology, ZMNH, University MC, Hamburg-Eppendorf, Hamburg, 20251, Germany |
| Additional literature: | RNAi knockdown of Crk, Crk-L or both induces alteration in the number of AChR clusters and their complexity in murine C2C12 myotubes. Knockdown of both was required to induce a significant effect, suggesting that both proteins can compensate for the absence of the other, and this is partially rescued by overexpression of CrkL. @ PMID:26527617 |
| SynGO annotation ID: | 3731 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |