ZAP70 pTyr493 Rabbit antibody Ab Aff - Purified
- Known as:
- ZAP70 pTyr493 Rabbit (anti-) Antibody Aff - Purified
- Catalog number:
- A7256-2
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ZAP70 pTyr493 Rabbit antibody Aff - Purified
Related genes to: ZAP70 pTyr493 Rabbit antibody Ab Aff - Purified
- Gene:
- ZAP70 NIH gene
- Name:
- zeta chain of T cell receptor associated protein kinase 70
- Previous symbol:
- SRK
- Synonyms:
- ZAP-70, STD
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-16
- Date modifiied:
- 2019-04-23
Related products to: ZAP70 pTyr493 Rabbit antibody Ab Aff - Purified
Related articles to: ZAP70 pTyr493 Rabbit antibody Ab Aff - Purified
- Acute Myeloid Leukemia (AML) is driven by complex interactions between genetic mutations and epigenetic dysregulation. While alterations in chromatin modifiers are frequent, the precise downstream transcriptional networks they enable and how these networks execute the leukemogenic program remain incompletely defined. - Source: PubMed
Publication date: 2026/05/30
Zeng LihuaLei HaohaoBi JingnanRun GuoweiYu BizhenJi Linhua - Zeta-chain-associated protein kinase 70 kDa (ZAP70) is a tyrosine kinase essential for T cell activation and differentiation and it is predominantly expressed in T cells. However, its clinical relevance and relationship with the immune microenvironment in lung adenocarcinoma (LUAD) remain unclear. Therefore, this study aimed to investigate the expression profile of ZAP70 in LUAD, evaluate its prognostic significance, and explore its correlation with the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/03/20
Zhang LunqiangLi XiuyingJin Fang - NK cells are the core cells of the innate immune system, which can kill cancer cells non-specifically and almost do not cause immune rejection or neurotoxicity, thereby enabling broad application in immune cell therapy. The KLRG1/Cadherin signaling axis has been reported to inhibit the anti-tumor response of NK cells. However, the mechanism by which KLRG1 regulates CAR NK cell function remains unclear. - Source: PubMed
Publication date: 2026/05/14
Chen YiranFarooq Muhammad AsadHui XinhuiHuang YunheHu YueXue MinAjmal IqraRen YaojunJi YuzhouWang ChenJiang Wenzheng - Wiskott-Aldrich Syndrome protein (WASp) is an actin nucleation-promoting factor that regulates the dynamic rearrangements of the actin cytoskeleton following T cell receptor (TCR) engagement. Recognition of antigen by T cells leads to TCR signal transduction, which involves the phosphorylation of various proteins in close proximity to the TCR, known as proximal TCR signalling. Proximal TCR signalling is initiated by the phosphorylation of signalling proteins including CD3 subunits, lymphocyte-specific protein tyrosine kinase (Lck) and zeta-chain-associated protein kinase 70 (ZAP70). Activation of these proteins initiates the formation of a signalosome, which is required for actin polymerisation and gene expression. The role of WASp in relation to proximal TCR signalling is largely unknown. In the present study, we knocked out WASp in Jurkat T cells using the CRISPR-Cas9 system to evaluate its effect on proximal TCR signalling. As expected, Jurkat T cells lacking WASp exhibited impaired actin polymerisation. Following TCR triggering, phosphorylation of CD3, Lck and ZAP70 was markedly reduced. There was also a failure in the recruitment of Lck and ZAP70 to the TCR. Impaired proximal TCR signalling (reduced tyrosine phosphorylation of CD3, Lck and ZAP70) was exclusively associated with decreased CD69 and CD25 expression. Therefore, besides its role in actin rearrangement, WASp is also required for proximal TCR signalling. - Source: PubMed
Publication date: 2026/05/13
Rattanasri ArayaChanaphai WilawanNuiyen AussaneePaensuwan PussadeePongcharoen SutatipNogenkam Jatuporn - Bladder cancer (BC) is a highly prevalent malignant tumor. The traditional Chinese medicine formula Guo Lou Qu Mai Wan (GLQMW), when used in conjunction with chemotherapy, has been shown to reduce adverse reactions and prolong survival time, although its specific mechanisms remain unclear. This study aims to investigate whether GLQMW exerts its therapeutic effects on bladder cancer by modulating the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/04/15
Teng QiliangCheng ShuminChen JiaZhu HongyaHu KaiSun LinglingZhao JinYuan ZhenboWang WenjingZhang LiLiu TaoliFeng Jiahao