| ID | Sequence | Length | GC content |
|---|---|---|---|
| ACACAAGUUGUAGAUGGCCUUCAGAUAUCCAAGGGGAGGCGUCCAGGAG… | 2557 nt | 0.6101 | |
| AGAUAUCCAAGGGGAGGCGUCCAGGAGGUAGUUGGGUUUCCAAGUCUGG… | 2806 nt | 0.6119 | |
| CCCGCUCCUCCCCCGACAAGGCGAUGAGGUAAUCGCGCCGCUGAGAGGC… | 2694 nt | 0.6229 | |
| GAUGAGGUAAUCGCGCCGCUGAGAGGCACGCGCAGCCGGUGCCUAGCCG… | 2666 nt | 0.6215 | |
| GAGAAAGGCAGGAGCCGCUGGGUUUAGGAGGUCCCCGGGUUGCCGGCGG… | 2977 nt | 0.6191 | |
| GAGAAAGGCAGGAGCCGCUGGGUUUAGGAGGUCCCCGGGUUGCCGGCGG… | 2606 nt | 0.6186 | |
| ACUCGCAAGCUGGCCAAGGGCUUCACACAAUUUGCCAAGAUGACAGAGG… | 3051 nt | 0.6083 |
This gene encodes an adaptor protein and member of a cytoplasmic protein family involved in cell migration. The encoded protein contains a putative Src homology 2 (SH2) domain and guanine nucleotide exchange factor-like domain which allows this signaling protein to form a complex with scaffolding protein Crk-associated substrate. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Nov 2011]
A study in humans demonstrated that the SH2D3C is an adapter protein mediating cell signaling for adhesion, migration, and immune response, and its expression shows a down-regulated pattern after death, where it was included in a post-mortem interval (PMI) prediction model with a negative coefficient [Antiga et al. DOI:10.1038/s41598-021-96095-z]. In a separate human study on myocardial ischaemia reperfusion injury, the SH2D3C mRNA was identified as a potential transcriptional regulator significantly enriched in the cellular response to stress, presented a negative correlation with injury, and its down-regulation reduced cardiac microvascular endothelial cell viability in an *in vitro* hypoxia/reoxygenation model [Liu et al. DOI:10.1111/jcmm.14163].