SHC4 Antibody (N-term)
- Known as:
- SHC4 Antibody (N-terminus)
- Catalog number:
- AP11930a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SHC4 Antibody (N-term)
Related genes to: SHC4 Antibody (N-term)
- 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 (N-term)
Related articles to: SHC4 Antibody (N-term)
- Ferroptosis, an iron-dependent form of regulated cell death, plays a pivotal role in hepatocellular carcinoma (HCC) progression and is now recognized as a key mechanism underlying the antitumor activity of sorafenib. Src homology and collagen protein 4 (SHC4), an adaptor protein implicated in oncogenic signaling and tumor progression, has recently emerged as a potential regulator in multiple cancers; however, its involvement in ferroptosis and sorafenib response remains unclear. Our preliminary data showed that sorafenib treatment alters SHC4 expression in both clinical tissues and HCC cell models, suggesting a possible connection between SHC4 and ferroptotic susceptibility. These findings prompted us to investigate whether SHC4 modulates ferroptosis and contributes to sorafenib resistance. Here, we found that SHC4 decreased the anti-tumor activity of sorafenib by reducing ferroptosis both in vitro and in vivo. SHC4 diminished ROS and MDA production, lowered intracellular iron levels, enhanced GSH levels, and regulated the expression of Nrf2, xCT, and GPX4 proteins associated with antioxidant stress. In addition, SHC4 interacts with the 383-522 fragment of NCOA4, thereby blocking the association between NCOA4 and FTH1. This interference reduces the lysosomal degradation of FTH1, leading to decreased intracellular Fe levels and ultimately suppressing ferroptosis. Clinically, the concurrent overexpression of SHC4 and FTH1 has been identified as a potential prognostic marker for poor outcomes in patients with hepatocellular carcinoma. Collectively, our study demonstrates the pivotal role of SHC4 in regulating ferroptosis in hepatocellular carcinoma and highlights its potential as a novel therapeutic target for overcoming sorafenib resistance. - Source: PubMed
Publication date: 2026/06/27
Chai DongqiZhang JiachengDong KeshuaiYu JiaZhang XinKuang TianruiFeng JiaruiLi ManWang Weixing - 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