Shc1 (Phospho_Tyr427) Antibody
- Known as:
- Shc1 (Phospho_Tyr427) Antibody
- Catalog number:
- E011317-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Shc1 (Phospho_Tyr427) Antibody
Related genes to: Shc1 (Phospho_Tyr427) Antibody
- Gene:
- SHC1 NIH gene
- Name:
- SHC adaptor protein 1
- Previous symbol:
- SHC
- Synonyms:
- p66, ShcA
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-17
- Date modifiied:
- 2016-10-05
Related products to: Shc1 (Phospho_Tyr427) Antibody
Related articles to: Shc1 (Phospho_Tyr427) Antibody
- This study aimed to compare ethnicity-related differences in DNA methylation profiles during metabolic dysfunction-associated steatohepatitis (MASH)-related hepatocarcinogenesis in patients from Japan and the United States (US). Genome-wide DNA methylation analysis using the Infinium assay was performed in 36, 148 and 36 samples of normal liver tissue (NLT), non-cancerous liver tissue showing MASH, and MASH-related hepatocellular carcinoma (HCC), respectively (220 samples in total), from the Japan and US cohorts. Principal component analysis revealed that MASH had a distinct DNA methylation profile differing from that of NLT, and that the MASH profiles in the two cohorts differed from each other. DNA methylation alterations of cancer-related genes in MASH were inherited by or strengthened in MASH-related HCC itself, resulting in expression alterations. DNA methylation alterations of FGFR2, FUT4, B3GNT5 and MOSC1 in the precancerous MASH stage were shared by the two cohorts, suggesting that such genes are commonly associated with MASH-related hepatocarcinogenesis. On the other hand, it was suggested that DNA methylation alterations of ZNF611 and SAMD10, and those of SHC1, are involved specifically in MASH-related hepatocarcinogenesis in the Japan and the US cohorts, respectively. These findings suggest that DNA methylation alterations, which may reflect race and lifestyle, are associated with MASH-related hepatocarcinogenesis. - Source: PubMed
Publication date: 2026/06/20
Kuramoto JunkoArai EriFujimoto MaoMuramoto HirokiOjima HidenoriSeki YosukeKasama KazunoriFunahashi NobuakiUdagawa HaruhideNammo TakaoYasuda KazukiHiraoka NobuyoshiYoshida TeruhikoEvason Kimberley JaneKanai Yae - Chronic myeloid leukemia (CML) is a myeloproliferative disorder driven by the fusion protein p210 BCR-ABL. In addition to activating canonical cytosolic signaling pathways, p210 BCR-ABL has been shown to translocate to the mitochondria upon mitochondrial damage through the interaction between its pleckstrin homology domain and cardiolipin, a mitochondria-specific phospholipid. We recently demonstrated that a fraction of p210 BCR-ABL localizes to the mitochondria in CML cells and promotes cell survival through mitochondria-associated signaling. However, whether mitochondria translocation of p210 BCR-ABL affects the major downstream signaling pathways activated by p210 BCR-ABL remains unclear. Here, we investigated the effects of mitochondrial translocation of p210-BCR-ABL on the JAK2/STAT5-, PI3K/AKT-, and RAS/MAPK-pathways using HEK293T cells expressing p210 BCR-ABL. Carbonyl cyanide m-chlorophenylhydrazone (CCCP), which induces mitochondrial damage and subsequent mitochondrial translocation of p210 BCR-ABL, markedly reduced ERK activation, whereas STAT5 and AKT activation were largely unaffected. Consistently, phosphorylation of SHC1, an adaptor protein directly phosphorylated by p210 BCR-ABL and required to ERK activation, was also suppressed by CCCP treatment. In contrast, CCCP did not affect EGF-induced ERK activation, indicating that the observed effect was specific for p210 BCR-ABL signaling. Moreover, N-acetylcysteine inhibited CCCP-induced reactive oxygen species production, prevented mitochondrial translocation of p210 BCR-ABL, and fully restored ERK-activation. These findings suggest that intercellular relocation of p210 BCR-ABL dynamically rewires downstream signaling networks, potentially optimizing the signaling balance required for CML cell survival and proliferation. - Source: PubMed
Publication date: 2026/06/17
Okuda YutaWatanabe-Takahashi MihoNishikawa Kiyotaka - Advanced and recurrent cervical cancer (CC) remains a clinical challenge due to limited therapeutic options and a poor 5-year survival rate (<20%). While immunotherapy has reshaped the treatment landscape, primary resistance driven by immune exclusion often limits its efficacy. This study aims to identify the key molecular determinants governing T-cell infiltration and to develop a robust prognostic framework by systematically analyzing the cancer immunoediting process. - Source: PubMed
Publication date: 2026/05/19
Ling Hong-JianZhou Jia-LiCao Lu-QiLi RyanChen Zhe-ShengYi Qiang - During final cell division, the cleaved midbody is either released or asymmetrically retained as a midbody remnant (MBR). MBRs play critical roles in cell communication, signal transduction, and translation regulation, influencing cellular fate. Here, we synthesize their functions as RNA-processing granules, polarity regulators, and signaling platforms, emphasizing their role in primary cilia formation. In polarized epithelial cells, the MBR moves along the apical surface to the centrosome, delivering membrane components to permit ciliogenesis. In ductal carcinoma cells, MBR-localized Shc1-binding protein (SHCBP1) interacts with TBC1 domain family member 30 (TBC1D30 to antagonize Ras-related protein Rab-8 (Rab8) GTPase activity, blocking MBR-centrosome proximity and silencing ciliogenesis. Beyond ciliary regulation, MBRs integrate Wnt, PDGF, TGF-, and genomic stability networks, acting as dynamic signaling hubs during cancer development. Regarding therapeutic strategies targeting MBRs, High SHCBP1 expression correlates with ciliary loss and poor prognosis in breast, pancreatic, and cholangiocarcinoma. Targeting the SHCBP1/Rab8 axis to restore ciliogenesis by reestablishing MBR-centrosome proximity offers a potential therapeutic strategy. In addition, secreted MBRs are enriched in signaling components and transcripts, serving as intercellular carriers of oncogenic cargoes and promising liquid biopsy biomarkers. In summary, by tracing MBRs from their postmitotic origin to their pathogenic roles, we highlight vulnerabilities within MBR regulatory networks and provide novel insights for cancer therapeutics. - Source: PubMed
Publication date: 2026/05/04
Li HongbinMa XiaoliLiang JingXue KaiShi WenguiLang Wanying - Nonobstructive azoospermia (NOA) is one of the most severe types of male infertility. Amino acid metabolism (AAM) is strongly associated with various diseases. This study intended to identify biomarkers related to AAM in NOA. Biomarkers were screened from GSE9210, GSE108886, and AAM-related genes through a series of bioinformatics analyses. Then, the diagnostic efficacy of the biomarkers was evaluated. Furthermore, the mechanisms of action of these biomarkers were investigated through enrichment analysis, immune infiltration analysis, construction of regulatory networks, prediction of potential drugs, and prediction of related diseases. Finally, reverse transcription-quantitative polymerase chain reaction was performed for verification. Three biomarkers (AKT1, ASNS, and SHC1) were derived, which demonstrated good diagnostic efficacy for NOA. Meanwhile, AKT1, ASNS, and SHC1 might play significant roles in the development of male germ cells through pathways such as male gamete generation, sexual reproduction, and gamete generation. Immune infiltration analysis revealed these 3 biomarkers were closely associated with T follicular helper cells, resting natural killer cells, and regulatory T cells. And AKT1, ASNS, and SHC1 were regulated by 24 transcription factors and 15 microRNAs. Remarkably, sodium selenite, aflodac, and genistein were commonly predicted by the biomarkers. In addition, lung neoplasms were associated with AKT1, lipoidosis was associated with ASNS, and drug-induced acute liver injury was associated with SHC1. Ultimately, AKT1 and SHC1 were significantly upregulated in NOA. This study identified 3 biomarkers as being associated with NOA, providing valuable clues to help treat and predict NOA. - Source: PubMed
Guo Qing HuaDing Zhong JunLiu Dong MeiRen Xiao ShanChen XiaoYong