STK17A polyclonal antibody
- Known as:
- STK17A pab (anti-)
- Catalog number:
- PAB9860
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- STK17A polyclonal antibody
Related genes to: STK17A polyclonal antibody
- Gene:
- STK17A NIH gene
- Name:
- serine/threonine kinase 17a
- Previous symbol:
- -
- Synonyms:
- DRAK1
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2014-11-19
Related products to: STK17A polyclonal antibody
Related articles to: STK17A polyclonal antibody
- Pancreatic ductal adenocarcinoma (PDAC) frequently harbors co-occurring alterations in KRAS, TP53, CDKN2A, and SMAD4, yet how clinically prevalent driver combinations shape kinase dependencies remains incompletely understood. To systematically interrogate genotype-dependent and shared vulnerabilities, we generated Drosophila models representing dominant PDAC driver contexts, including 2-hit (KRAS-TP53) and 3-hit (KRAS-TP53-CDKN2A or KRAS-TP53-SMAD4) genotypes, and conducted comparative whole-animal genetic screening using organismal viability as a phenotypic readout. This approach identified both genotype-specific modifiers and a subset of kinases whose suppression consistently improved viability across distinct genetic contexts, enabling prioritization of conserved candidates for cross-species validation. Among these, the Drosophila kinase Drak, orthologous to human STK17A/STK17B, emerged as a recurrent shared vulnerability. Functional validation in three-dimensional spheroid cultures of human PDAC cell lines representing distinct driver genotypes demonstrated that STK17B perturbation impairs spheroid growth across models. Transcriptomic profiling further revealed coordinated downregulation of gene sets linked to DNA replication and E2F-driven cell-cycle programs upon STK17B knockdown. Together, these findings establish a genotype-informed screening framework for systematic discovery of shared and context-dependent kinase dependencies in PDAC, and nominate STK17B as a conserved genetic vulnerability across dominant driver contexts. - Source: PubMed
Publication date: 2026/09/01
Hai HanOoshio TakakoJiang HuiKimura TakuSatoh YusukeHata SoichiroHirata TaigaLiu JiayiLiu TongweiYamamura RyodaiSonoshita Masahiro - Death-associated protein kinase-Related Apoptosis-inducing protein Kinase 1 (DRAK1/STK17A) is a serine/threonine kinase of the Death Associated Protein Kinase (DAPK) family. STK17A is widely expressed and enriched in immune tissues, and is primarily localized in the nucleus, though it can translocate to the cytoplasm in response to specific stimuli. STK17A stimulates apoptosis and cytoskeletal dynamics, but its physiological roles remain incompletely defined, in part due to limited availability of potent/selective chemical probes and the absence of STK17A in commonly used rodent models. In this review, we summarize current knowledge on STK17A, including its structure, evolution, expression patterns, molecular interactions, and roles in cancer as well as in autoimmune, cardiovascular, infectious, and neurological disorders. We also compare STK17A with its closest homolog, STK17B, highlighting both shared features and functional distinctions. The review further examines recent medicinal chemistry efforts that have yielded the first small-molecule modulators of STK17A (DRAK1) and STK17B (DRAK2), including dual inhibitors and emerging selective scaffolds. These compounds can serve as valuable chemical probes and hold promising therapeutic potential. Nonetheless, challenges of selectivity and functional validation remain, emphasizing the need for continued medicinal chemistry efforts to unlock the full potential of STK17A as a therapeutic target across cancer, autoimmune, and neurodegenerative diseases. - Source: PubMed
Publication date: 2026/03/30
Gonçalves Leticia Christina PiresRastoin OliviaMorozova ViraBuzet ClémentBennetot AudreyPagès GillesRonco CyrilDufies Maeva - Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Fig. 11A on p. 279, these plots appeared to show similar groupings of dots, which would not have been anticipated if these experiments had been performed discretely under different experimental conditions, suggesting a fundamental flaw either in the way in which these experiments were performed or in how the results were outputted. The Editor of has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 21: 267‑281, 2020; DOI: 10.3892/mmr.2019.10826]. - Source: PubMed
Publication date: 2026/04/24
Wei WeiLiu Cun - PFOA and NPs are recognized as persistent organic pollutants with potential ecological risks in aquatic ecosystems, and they exhibit specific toxic effects on benthic invertebrates. As a vital respiratory organ of aquatic animals, the gill plays a key role in gas exchange and osmoregulation. However, studies on the potential adverse impacts of these two pollutants on the gill tissue remain scarce. In the present study, we conducted a 28-day stress experiment with the Eriocheir sinensis as a research model and systematically investigated the toxic effects of PFOA/NPs on gill organs by multi-omics sequencing. At the biochemical level, PFOA/NPs inhibited the activity and transcription of antioxidant enzymes (CAT, T-SOD, and GSH) or genes (gpx, gstd7), while triggering oxidative stress (MDA) and causing morphological damage. Moreover, PFOA/NPs induced inflammation (TNF-α, hil-6), apoptosis, autophagy (bnip3, stk17a, lc3a, epg5), suppression of immune responses (fcn, lyz), and disruption of glycolipid metabolism (fasn, acsl14, srebf1, acsly). In addition, the PFOA-NPs co-exposure disrupted the microbial flora structure in gill tissues, including reduced community evenness, increased dominance of specific species, and heightened abundances of both environmental organic pollutant-degrading microbes and opportunistic pathogens (Acidovorax, Sphaerotilus, Candidatus_Bacilloplasma). Furthermore, PFOA-NPs may disrupt microbial physiological homeostasis by suppressing the "LPS biosynthesis-antibiotic production-GAG degradation-lysosomal function" axis. These findings indicate that the gill organs of aquatic crustaceans are highly sensitive to organic pollutants such as PFOA and NPs, and long-term exposure disrupts their tissue physiology and microbial community homeostasis, thereby providing critical data to support the ecotoxicological assessment of PFOA/NPs in aquatic ecosystems. - Source: PubMed
Publication date: 2026/03/03
Huang PengGao JiancaoCao LipingLi JiayiDu JinliangXu Gangchun - STK17A (serine/threonine kinase 17a), also known as DRAK1 (death-associated protein kinase-related apoptosis-inducing protein kinase 1), is a member of the death-associated protein kinase (DAPK) family and acts as a positive regulator of apoptosis. STK17A is a dark kinase and is an understudied member in the DAPK family. Thus far, it has been found to serve a significant role in cell proliferation, apoptosis, tumor metastasis, and tumorigenesis. This review summarizes the structure of STK17A, its reported biological functions, and expression in cancer. Small molecule inhibitors for STK17A, including those specifically developed for STK17A and those designed for other kinases but also inhibit STK17A as an unintended target, are discussed. Finally, some outlooks for drug discovery regarding STK17A are described. - Source: PubMed
Publication date: 2025/12/12
Ouaakki HafsaBravo EduardoTaylor JustinFeng Yangbo