Ask about this productRelated genes to: SHC4 antibody
- Gene:
- SHC4 NIH gene
- Name:
- SHC adaptor protein 4
- Previous symbol:
- -
- Synonyms:
- RaLP, SHCD
- Chromosome:
- 15q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-07
- Date modifiied:
- 2016-10-05
Related products to: SHC4 antibody
Related articles to: SHC4 antibody
- Only a subset of individuals infected with SARS‑CoV‑2 develop severe COVID‑19. Improved tools for early diagnosis and prognostication are needed. We hypothesized that unsupervised analysis of detailed circulating proteomes could reveal biologically meaningful patient endotypes and help identify individuals at elevated risk of severe outcomes. - Source: PubMed
Publication date: 2026/03/14
Ma WilliamSoulé AntoineAllard CatherineDurand MadeleineTremblay KarineRousseau SimonEmad Amin - Esophageal cancer has remained a therapeutic challenge despite the advancements in targeted therapy and immunotherapy. This study investigated the mechanism by which neoadjuvant pembrolizumab combined with carboplatin and varying dosages of albumin-bound paclitaxel (ABP) regulates immune microenvironment in esophageal cancer. In vivo, a homograft mouse model was constructed. Both combined treatment groups displayed considerably decreased tumor volume (P < 0.001). Furthermore, the combined treatment inhibited tumor progression by downregulating SHC adaptor protein 4 (shc4) expression, and modulating immune cell homeostasis, as evidenced by remarkably reduced T helper Th1/Th2 and Th17/Regulatory T (Treg) ratios (P < 0.05). Cytokine analysis data revealed that levels of neutrophil cytosolic factor 2 (Ncf2) and related factors were higher in the two combined treatment groups than the Model group (P < 0.05). This study demonstrates that neoadjuvant combination therapy inhibits esophageal cancer progression by reshaping the immune landscape. - Source: PubMed
Publication date: 2025/12/26
Liang GaofengYu HongyanWu ShengqianShen WeiyuHe Jinxian - Shc family adaptor proteins are involved in diverse signaling pathways that regulate critical cellular functions, including proliferation, differentiation, migration, and survival. ShcD is the most recently isolated member and while previous studies have identified its prominent expression in the brain, specifically within the olfactory bulb, its physiological functions remain largely unknown. Here we report initial characterization of ShcD knockout (ShcD) mice and identify structural, behavioral, and biochemical deficits associated with ShcD deletion. Specifically, ShcD mice have decreased olfactory bulb weight with a corresponding reduced granule cell layer compared to controls, and defects in olfactory performance. Intriguingly, ShcD mice display increased proliferation in the subventricular zone, which serves as the reservoir for neural progenitors migrating into the olfactory bulb. Supporting these cellular changes, we noted Erk2 hyperactivation in the olfactory bulb of ShcD mice, and using a cultured neuron model, we also detected altered signaling of Erk5, a MAPK protein associated with neural stem cell differentiation, as well as increased p66ShcA expression, indicating a potential compensatory mechanism within the Shc family. These results uncover a possible physiological role for ShcD in neurogenesis and imply its involvement in signaling pathways that regulate stem cell maintenance and/or differentiation. - Source: PubMed
Publication date: 2025/12/15
Robeson Hannah NNew Laura AAlural BegümClausen CassandraErvin Kelsy S JYang HyeyunCooper C JamesCholeris ElenaLalonde JasminJones Nina - Triple-negative breast cancer (TNBC) is highly metastatic and presents clinical challenges given the lack of targeted therapies. Here, we report that the ShcD phosphotyrosine adaptor protein is upregulated in TNBC, and its expression correlates with overall reduced patient survival and decreased response to chemotherapy. In human breast cancer cells, we demonstrate that ShcD expression promotes cell invasion and reduces adhesion, and that these effects are abrogated by mutating the ShcD phosphotyrosine binding (PTB) domain. Similarly, in a three-dimensional assembloid model, ShcD-expressing spheroids derived from brain metastatic TNBC cells show enhanced infiltration into cerebral organoids. Using a proteomic screen for ShcD binding partners, we identify multiple components of epidermal growth factor receptor (EGFR) signaling and confirm these interactions with ShcD but not the PTB mutant. Interestingly, the ShcD interactome correlates with EGFR tyrosine kinase inhibitor resistance, in line with our findings that ShcD overexpression results in hyperphosphorylation of EGFR while ShcD knockout or PTB mutation reverts this response. Lastly, pharmacological inhibition of the ShcD PTB domain using indomethacin in TNBC cells decreases EGFR binding and hyperphosphorylation and reduces cell invasion. Altogether, our results identify ShcD as a potential contributor to metastasis in TNBC, and they provide a molecular basis for clinical targeting of adaptor proteins. - Source: PubMed
Publication date: 2025/03/28
Lau Hayley RSmith Hayley SAlural BegümMartin Claire ENew Laura ATilak ManaliBanerjee Sara LRobeson Hannah NBisson NicolasGingras Anne-ClaudeLalonde JasminJones Nina - Cutaneous squamous cell carcinoma is one of the most common cancers in humans and kills as many people annually as melanoma. The understanding of the transcriptional changes with respect to high-risk clinical/histopathologic features and outcome is poor. In this study, we examine stage-matched, outcome-differentiated cutaneous squamous cell carcinoma using whole-exome and transcriptome sequencing. Exome analysis identified key driver mutations, including TP53, CDKN2A, NOTCH1, SHC4, MIIP, CNOT1, C17orf66, LPHN2, and TTC16, and pathway enrichment of driver mutations in replicative senescence, cellular response to UV, cell-cell adhesion, and cell cycle. Transcriptomic analysis identified pathway enrichment of immune signaling/inflammation, cell-cycle pathways, extracellular matrix function, and chromatin function. Integrative analysis identified 183 critical genes in carcinogenesis and were used to develop a gene expression panel for outcome. Three outcome-related gene clusters included those involved in keratinization, cell division, and metabolism. We found 16 genes whose expressions may be associated with metastasis (risk score ≥ 9 Met and risk score < 9 NoMet) with an area under the curve of 97.1%, sensitivity of 95.5%, specificity of 85.7%, and overall accuracy of 90%. Eleven genes were chosen to generate the risk score for overall survival, with an overall survival prediction of 80.8% and each risk gene increasing the risk of death by 2.47 (hazard ratio = 2.47, P < .001). - Source: PubMed
Publication date: 2025/01/28
Nassir ShamsYousif MirandaLi XingSeverson Kevin JHughes AlysiaKechter JacobHwang AngelinaBoudreaux BlakeBhullar PuneetZhang NanButterfield Richard JMa TaoLeibovit-Reiben ZacharyStockard AlyssaOgbaudu EwomaCostello Collin MNelson Steven ADiCaudo David JSekulic AleksandarBaum Christian LPittelkow Mark RMangold Aaron R