DRAK2 pAb;human
- Known as:
- DRAK2 pAb;H. sapiens
- Catalog number:
- ASAAAP-432E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- DRAK2 pAb;human
Related genes to: DRAK2 pAb;human
- Gene:
- STK17B NIH gene
- Name:
- serine/threonine kinase 17b
- Previous symbol:
- -
- Synonyms:
- DRAK2
- Chromosome:
- 2q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2016-10-05
Related products to: DRAK2 pAb;human
Related articles to: DRAK2 pAb;human
- 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 - Natural killer (NK) cells are promising effectors for cancer immunotherapy, but their efficacy is limited by immunosuppressive tumor microenvironments. To uncover strategies for enhancing NK cell function, we establish a CRISPR loss-of-function screening platform for primary human NK cells by combining BaEVRless-pseudotyped lentiviral transduction of sgRNA libraries with Cas9 protein electroporation. This platform enables genome-scale interrogation of gene function in non-transformed NK cells. Kinome-focused and genome-wide screens identify key regulators of NK cell proliferation, cytotoxicity, and resistance to prostaglandin E (PGE)-mediated suppression. STK17B deletion enhances NK cell expansion, while loss of CCDC53 boosts degranulation and cytotoxicity. We also uncover the CRL5 complex-including RNF7, UBE2F, and CISH-as critical inhibitors of IL-2 signaling and effector function under PGE stress. These findings establish a scalable platform for CRISPR-based functional genomics in primary NK cells and reveal engineering targets to enhance NK cell persistence and efficacy in tumor microenvironments. - Source: PubMed
Publication date: 2026/04/15
Nguyen Quoc VietLan Yi-JunChang Jason Cheng-YuShih Hsin-AnFaustine JeniferChen Cheng-ChiehHo Shu-YuCheng Ching-WenChao Tsu-LanLin Steven - [This corrects the article DOI: 10.21037/atm-21-601.]. - Source: PubMed
Publication date: 2025/01/15
- - Source: PubMed
Liu Bei - DRAK2 (STK17B), a serine/threonine kinase, plays a critical role in apoptosis and has been implicated in metabolic diseases, including type 2 diabetes (T2D) and metabolic dysfunction-associated steatohepatitis (MASH). Previous studies have demonstrated DRAK2's roles in pancreatic β cell dysfunction and mitochondrial impairment. This study is dedicated to the development of novel DRAK2 inhibitors aimed at preserving β cell function. Through comprehensive structure-activity relationship (SAR) analyses, we synthesized and evaluated a series of compounds, identifying potent inhibitors (represented by Y17) with nanomolar potency. In vitro experiments revealed that these compounds enhanced mitochondrial membrane potential (MMP) in INS-1E cells and glucose-stimulated insulin secretion (GSIS) in primary mouse islets, as well as protecting against palmitic acid (PA)-induced apoptosis. In vivo studies demonstrated the distribution of the compounds in pancreatic tissue and their ability to improve glucose tolerance in mice. Molecular docking analyses elucidated key interactions between the inhibitors and DRAK2. The inhibitors exerted their function particularly via the DRAK2-ULK1 axis, thereby confirming their mechanism of action. Collectively, our findings underscore DRAK2 as a promising therapeutic target for T2D and provide a potential for developing antidiabetic therapies through preserving β cell function. - Source: PubMed
Publication date: 2025/10/12
Lian KaiyueLi RuihanLu YutingSong GaoleiZhang XinwenZhang YuxinXu HonghongSun XinyuGu MinYang YangMa HuiLi JingyaNan Fajun