Gab1 Antibody (Phospho-Tyr627), pAb, Rabbit
- Known as:
- Gab1 Antibody (Phospho-Tyr627), pAb, Rabbit
- Catalog number:
- A00568-100
- Product Quantity:
- 100,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- Gab1 Antibody (Phospho-Tyr627) pAb Rabbit
Related genes to: Gab1 Antibody (Phospho-Tyr627), pAb, Rabbit
- 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 Antibody (Phospho-Tyr627), pAb, Rabbit
Related articles to: Gab1 Antibody (Phospho-Tyr627), pAb, Rabbit
- 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 - Lung adenocarcinoma (LUAD) is the main histologic subtype of lung cancer, and its incidence is on the rise. However, since the vast majority of patients are already in advanced stages at the time of diagnosis, their 5-year survival rate is only 15%, so it is urgent to explore the mechanism of the development of LUAD and improve the survival time of patients. Interleukin-11 (IL-11), a member of the IL-6 cytokine family, has an influential role in the development and progression of a variety of tumors, but the specific molecular mechanisms that promote the malignant progression of LUAD are unknown. Here, we found that the IL-11-induced activation of Akt, Erk, and STAT3 could be inhibited by knocking out the expression of Gαi1/3. In contrast, overexpression of Gαi1/3 could enhance IL-11-induced signaling. The binding of Gαi1/3 to GP130 mediates IL-11-induced downstream activation of Akt-mTOR, Erk, and STAT3, which requires recruitment of Grb2-associated binding protein 1 (Gab1). In LUAD cells, shGαi1/3 inhibited cell growth, proliferation, and migration as well as blocked the tumor-promoting ability of IL-11. However, overexpression of Gαi1/3 enhanced the IL-11-induced cell growth, proliferation, and migration. ShGαi1/3 also inhibited the proliferation of LUAD cells in vivo. Overall, the findings of this study demonstrate the Gαi1 and Gαi3 are critical for IL-11 signal transduction. Moreover, we reveal that Gαi1 and Gαi3 are highly expressed and associated with poor overall survival in lung adenocarcinoma and may thus act as potential therapeutic targets in LUAD. These results provide a novel therapeutic strategy for LUAD patients with upregulated IL-11 expression. - Source: PubMed
Publication date: 2026/04/25
Luo GaomengHu WenxuanYang JianLu ZhengCui YuanZeng WeibiaoDing HaoLi QifanChen ZhikeTong XinDing ChengXu ChunZhao Jun - Lung adenocarcinoma (LUAD) remains a leading cause of cancer mortality. Although targeted therapies and immunotherapies have improved outcomes, many patients exhibit limited responses due to primary or acquired resistance, underscoring the need to identify novel molecular targets. The Gab family of scaffolding adaptors, including GAB1 and GAB2, are recognized oncogenic regulators, whereas the role of GAB3, implicated in immune cell activation, is poorly defined in solid tumors. Here, we identify GAB3 as a novel tumor suppressor in LUAD. Pan-cancer analysis revealed frequent GAB3 downregulation, and high GAB3 expression was associated with favorable prognosis. Functionally, GAB3 overexpression suppressed LUAD cell proliferation, migration, invasion, and tumor growth in vitro and in vivo. Mechanistically, GAB3 interacted with LYN kinase to inhibit the MAPK signaling pathway and reverse epithelial-mesenchymal transition (EMT). In addition, GAB3 remodeled the tumor immune microenvironment, enhanced CXCL10 secretion, increased CD8 T cell infiltration and effector function, and potently sensitized tumors to anti-PD-1 therapy. Our findings support a dual tumor-suppressive mechanism for GAB3 and propose it as a promising prognostic biomarker and therapeutic target in LUAD. - Source: PubMed
Publication date: 2026/04/22
Wang DiXiao ChuFan TaoDeng ZiqinYin HongfeiLiu YixiaoLi JiaJi YuCai WenpengLiao TianleLi JiayanLi ChunxiangHe Jie - Molecular profiling is becoming crucial for accurate classification, prognostication, and therapeutic stratification for central nervous system (CNS) tumor classification since the advent of the WHO 2021 CNS tumor classification. However, in most of the low-income countries and middle-income countries, access to advanced molecular platforms remains limited due to cost, technical complexity, and turnaround time. Surrogate immunohistochemistry markers for mutation-specific or fusion-specific antibodies that reliably predict underlying genetic alterations offer a rapid, cost-effective alternative. The manuscript systematically discusses a spectrum of CNS tumor entities where morphology supplemented with immunohistochemistry can, in many cases, support an integrated molecular diagnosis, including "Astrocytoma, IDH-mutant" (IDH R132H, ATRX, and p53), "Oligodendroglioma, IDH-mutant, and 1p/19q codeleted" (HIP1R, H3K27me3 loss, and vimentin), "Diffuse midline glioma, H3K27-altered" (H3K27M, EZHIP), "Diffuse hemispheric glioma, H3G34-mutant" (H3G34R/V), "Infant-type hemispheric glioma" (Pan-TRK, ALK), "Epithelioid glioblastoma" and "Pleomorphic xanthoastrocytoma" (BRAF V600E)), "Astroblastoma, MN1-altered" (MN1), "Ependymoma" subtypes (p65, L1CAM, EZHIP), "Medulloblastoma" subgroups (β-catenin, LEF1, YAP1, GAB1), "Atypical teratoid/rhabdoid tumor" (SMARCB1, SMARCA4), "CNS neuroblastoma, FOXR2-activated" (FOXR2), "CNS tumor with BCOR ITD" (BCOR), and various sarcomas and sellar tumors (STAT6, NKX2.2, DUX4, β-catenin, BRAF V600E). For each entity, detailed morphologic features, immunoprofiles, sensitivity/specificity data, and diagnostic caveats have been described. The review emphasizes that when interpreted alongside histomorphology and conventional markers, surrogate immunohistochemistry can significantly reduce reliance on molecular testing, expedite diagnosis, and improve accessibility of precision diagnostics. Standardization, validation, and awareness of pitfalls remain essential to maximizing their clinical utility in neuropathology practice. - Source: PubMed
Publication date: 2026/04/09
Das SumantaSuri VaishaliAhlawat SunitaSharma Mehar C