Basic Information

Symbol
SH2D3C
RNA class
mRNA
Alias
SH2 Domain Containing 3C NSP3 SH2 Domain-Containing Eph Receptor-Binding Protein 1 Cas/HEF1-Associated Signal Transducer SH2 Domain-Containing Protein 3C Novel SH2-Containing Protein 3 Chat-H SHEP1 SH2 Domain-Containing 3C PRO34088 CHAT
Location (GRCh38)
Forensic tag(s)
Postmortem interval inference Sudden cardiac death diagnosis

MANE select

Transcript ID
NM_170600.3
Sequence length
3051.0 nt
GC content
0.6083

Transcripts

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
Summary

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]

Forensic Context

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].