Gab1 (Phospho_Tyr659) Antibody
- Known as:
- Gab1 (Phospho_Tyr659) Antibody
- Catalog number:
- E012082-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Gab1 (Phospho_Tyr659) Antibody
Related genes to: Gab1 (Phospho_Tyr659) Antibody
- Gene:
- GAB1 NIH gene
- Name:
- GRB2 associated binding protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-18
- Date modifiied:
- 2016-10-05
Related products to: Gab1 (Phospho_Tyr659) Antibody
Related articles to: Gab1 (Phospho_Tyr659) Antibody
- Retinal neovascularization (RNV) is a potential vision-threatening process characterized by the abnormal growth of retinal vessels. Despite its clinical prevalence, the precise mechanisms governing RNV initiation and progression remain incompletely defined. Here we identify myeloid-derived growth factor (MYDGF) as a critical regulator of retinal vascular dynamics. Using single-cell RNA sequencing and human patient validation, we show that MYDGF is upregulated in retinal endothelial cells during proliferative diabetic retinopathy and mouse models of pathological neovascularization. In vitro, MYDGF promotes retinal endothelial cell proliferation, migration, and sprouting. In vivo, endothelial-specific MYDGF depletion inhibits both normal vascular development and pathological neovascularization in neonatal mice, and disrupting adult vascular homeostasis in male mice. MYDGF drives angiogenesis by activating the Akt-mTOR cascade through the Gαi1/3-Gab1 signaling complex; genetic depleting or mutation these components suppress MYDGF-induced Akt-mTOR activation and angiogenic responses. Together, MYDGF promotes retinal angiogenesis and maintains vascular homeostasis via the Gαi1/3-Gab1-Akt-mTOR signaling axis. - Source: PubMed
Publication date: 2026/06/23
Li Ke-RanFu Ping-PingBai WenBai Chao-WenYang YitianLiu LeChai Jin-LongYao YujiaHuang DanZhang Zhi-QingJiang QinMa Zhou-RuiFeng YuYao JinCao Cong - Activation of Estrogen receptors (ER) signaling in adult male rats leads to sub-fertility, and whole genome bisulfite sequencing revealed large-scale genome-wide changes in sperm DNA methylation. In this study, we further probed the developmental consequences of altered sperm methylome. An enrichment map analysis of the differentially methylated genes revealed that clusters related to embryo development and its regulation were most enriched. Genes differentially methylated in sperm and implicated in embryo development were selected for validation in sperm by pyrosequencing. DNA methylation and expression levels of these developmental genes were evaluated in resorbed and normal embryos and placental tissues. The aberrant sperm DNA methylation pattern in developmental genes Cdkn1c, Tgfb1, Bmp4, Gab1, Peg3, Myc, Wt1, Sfmbt2, Sox5 and Hoxa3 was reflected in that of the resorbed embryos, along with their deregulated expression after paternal ER agonist treatment. Whereas, the methylation pattern and expression in normal embryos and placenta for most genes were comparable to those of the controls. Additionally, several key developmental pathways, including MAPK, Tgfβ, Wnt, Notch, Hedgehog, and Scf-cKit signaling, were also found to be affected in resorbed embryos sired by ERα agonist-treated male rats. The results indicate that activation of estrogen signaling during spermatogenesis causes aberrant sperm DNA methylation in developmental genes. These defects could be transmitted to embryos, altering the expression of these genes and pathways and thereby impeding embryonic development and reducing litter size and subfertility. The study provides a mechanism by which ERs epigenetically regulate male fertility and subsequent embryogenesis. - Source: PubMed
Publication date: 2026/06/11
Khambata KushaanRaut SanketaBalasinor Nafisa H - Prime editing (PE) enables precise nucleotide changes but has limited utility in high-throughput functional screening due to low editing efficiency. Here, we developed EvoPRIME, a PE3-based screening platform that integrates Csy4-mediated processing of Pol II-driven guide RNAs with a fluorescence-based enrichment strategy. EvoPRIME achieves comparable efficiency to state-of-the-art prime editing systems without requiring mismatch repair (MMR) suppression. We validated the performance of EvoPRIME through a loss-of-function (LOF) dropout screen targeting essential genes, which showed improved sensitivity and reproducibility, and a gain-of-function (GOF) saturation mutagenesis screen of the EGFR tyrosine kinase domain under osimertinib selection, which identified both known and uncharacterized resistance-conferring mutations. Leveraging EvoPRIME, we further conducted a high-throughput screen that functionally assesses both gain- and loss-of-phosphorylation (GOP and LOP) mutations. Among the hits, GAB1 S419E emerged as a phosphomimetic mutation that activates AKT signaling and confers osimertinib resistance. These studies establish EvoPRIME as a versatile platform for uncovering functional variants. - Source: PubMed
Publication date: 2026/06/05
Huang ShishengTao WanyuLi XiangyangGuo JunfanZhang YuLi GuangleiZhang PengfeiZhang GuiquanLi GaoyangFan GaofengZhang Shang-MinHuang Xingxu - Intrauterine adhesions (IUA) are fibrotic scars that impair endometrial regeneration, and compromise fertility. Emerging evidence implicates circular RNAs (circRNAs) in fibrotic remodeling, but it remains unclear how the circRNA landscape and circRNA-associated splicing programs coordinately link uterine contractility, endometrial cell-cycle control, and immune activation in IUA. - Source: PubMed
Publication date: 2026/05/07
Chen YingqingJin JingXiang YingWang YanpingWu ShuangZhan NiXiong MengxinDeng Ali - Despite the availability of RAS inhibitors and the dependence of >90% of pancreatic ductal adenocarcinomas (PDAC) on oncogenic KRAS mutations, resistance to KRAS inhibition remains a serious obstacle. We showed here that PI3K plays a major role in this resistance through upstream activation of wild-type RAS signaling - beyond its known KRAS effector function. The combination of proximity labeling, CRISPR screening, live-cell imaging, and functional assays revealed that PI3K orchestrates phosphoinositide-mediated GAB1 recruitment to the plasma membrane, nucleating assembly of RAS signaling complexes that activate MAPK in an EGFR/SHP2/SOS1-dependent manner. Inhibiting PI3K enhanced sensitivity to mutant-specific KRAS inhibitors in PDAC cells, including in cells with clinically identified PIK3CA mutations. These findings refine RAS-PI3K signaling paradigms, reveal that PI3K-driven wild-type RAS activation drives resistance to KRAS inhibition, and illuminate avenues for augmenting KRAS-targeted therapies in PDAC. - Source: PubMed
Publication date: 2026/05/07
Ge XiangyuSingh JaffarguriqbalLi WenxueMarkham Cassandra SRuiz Christian FelipeStites Edward CBhattacharyya MoitrayeeLiu YanshengMuzumdar Mandar Deepak