SH2D4A Antibody (N-term) Blocking Peptides
- Known as:
- SH2D4A Antibody (N-terminus) Blocking Peptides
- Catalog number:
- BP12049a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SH2D4A Antibody (N-term) Blocking Peptides
Related genes to: SH2D4A Antibody (N-term) Blocking Peptides
- Gene:
- SH2D4A NIH gene
- Name:
- SH2 domain containing 4A
- Previous symbol:
- -
- Synonyms:
- FLJ20967, SH2A, PPP1R38
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-16
- Date modifiied:
- 2016-10-05
Related products to: SH2D4A Antibody (N-term) Blocking Peptides
Related articles to: SH2D4A Antibody (N-term) Blocking Peptides
- Insulin-like growth factor binding protein-6 (IGFBP-6) is induced by progesterone in breast cancer cells and regulates progesterone receptor (PR) via negative feedback. To further understand the mechanisms by which IGFBP-6 regulates PR and downstream signaling, proteomic analysis was performed in progesterone-treated T47D breast cancer cells following siRNA-mediated knockdown of IGFBP-6. Of the 8638 unique proteins identified, 29 proteins were downregulated, and 14 proteins were upregulated by progesterone treatment after IGFBP-6 knockdown. The decreased proteins were mostly identified as regulators of G2/M phase of the cell cycle. SH2D4A is induced by progesterone only when IGFBP-6 was high. To understand the role of SH2D4A in progesterone-induced signaling, SH2D4A was knocked down using siRNA prior to progesterone treatment. Knockdown of IGFBP-6 or SH2D4A leads to cell cycle arrest in G1, and both SH2D4A and IGFBP-6 regulate cyclin B. Treatment of cells with abemaciclib and nocodazole caused cell cycle arrest in G1 and G2/M, respectively, and decreased IGFBP-6, suggesting that IGFBP-6 is regulated in a cell cycle-dependent manner. These results identify a pathway linking progesterone to IGFBP-6 and SH2D4A, and to cell cycle progression in breast cancer cells. - Source: PubMed
Publication date: 2026/06/30
Lariz Francisco JBautista-Tovar Diana CLazo-Loya AlejandroHouston Kevin D - Gastric cancer (GC) is a leading cause of cancer-related mortality globally, and elucidating the molecular drivers of its progression is essential for therapy development. The E3 ubiquitin ligase CBLC has been implicated in tumorigenesis, yet its role in GC remains undefined. - Source: PubMed
Publication date: 2026/05/12
Pan JingjingXiao Yiwen - Ruminant meat is an important component of human diets, valued for its unique flavor and nutritional density. Lipids play a dominant role in shaping meat flavor, yet their genetic and biochemical basis remains unexplored. Here, from the analysis of 434 sheep longissimus thoracis samples, the current study presents the first comprehensive lipid map of sheep meat, including 947 lipids. A substantial proportion of these lipids exhibit moderate-to-high heritability, with 51.6% surpassing a heritability of 0.2 and 15.8% exceeding 0.45. Metabolome-based genome-wide association analysis identifies 467 significant loci affecting 233 lipids, including 110 loci exhibiting pleiotropy. Notably, the levels of monogalactosyldiacylglycerols containing oleic (C18:1) and linoleic (C18:2) acids are specifically regulated by the expression of MBOAT1 and PAQR8 genes, respectively, while 13 triglycerides and one diglyceride are co-regulated by SH2D4A. The levels of phosphatidylethanolamine PE(20:4_20:0) are regulated by VPS53. Further examination of volatile compounds demonstrates that variations in these genetically controlled lipids significantly impact flavourant levels in cooked meat. Given the conservation of lipid profiles and genomes among ruminants, this study offers novel insights into the genetic architecture underlying meat lipid metabolism and provides a valuable resource for the targeted genetic improvement of ruminant meat flavor. - Source: PubMed
Publication date: 2025/08/11
Zhang XueyingKong YuanyuanChen JialeiLi RanWang ZhongyuSong YaliDai TianshuFu YuxinJiang BeixiangZeng JizePei ShengweiLiu YangkaiFeng QianjieFu WeiweiYuan ZehuMwacharo Joram MwashigadiLi FadiYue Xiangpeng - - Source: PubMed
Li ZiyaoXin ShiyongHuang LiqunTian YeChen WeihuaLiu XiangYe BowenBai RongYang GuoshengWang WenwenYe Lin - Clear cell renal cell carcinoma (ccRCC) is one of the most common malignancies. Recently, the role of brain-expressed X-linked 4 (BEX4) in cancer progression has received increasing attention. This study aimed to investigate the function of BEX4 in ccRCC and to reveal the underlying mechanisms. We first confirmed that BEX4 was significantly downregulated in ccRCC by bioinformatics analysis and that patients with low BEX4 expression tended to have prolonged overall survival time. Subsequently, we confirmed that BEX4 inhibited ccRCC cell proliferation in vitro and tumorigenesis in vivo through a series of cell function assays and the establishment of a nude mouse xenograft model, respectively. Mechanistically, we found that BEX4 positively regulates the expression of Src homology 2 domain-containing 4A (SH2D4A), an inhibitor of the NOTCH pathway, which further promoted the tumor-suppressive effects of BEX4. In addition, our study confirmed that the promoting effect of BEX4 on SH2D4A was achieved by inhibiting the deacetylase sirtuin 2 (SIRT2) activity. On this basis, we found that there was a competition between acetylation and ubiquitination modifications at the K69 site of SH2DA4 and that BEX4-induced upregulation of acetylation at the k69 site stabilizes SH2D4A protein expression by inhibiting ubiquitination at the same site. In addition, dual-luciferase assays showed that the transcriptional activity of BEX4 was positively regulated by activation transcription factor 3 (ATF3). Our study suggests that BEX4 plays a role in inhibiting tumor progression in ccRCC and maybe a new diagnostic and therapeutic target for ccRCC patients. - Source: PubMed
Publication date: 2024/12/05
Li ZiyaoXin ShiyongHuang LiqunTian YeChen WeihuaLiu XiangYe BowenBai RongYang GuoshengWang WenwenYe Lin