PDPK1 pTyr9 antibody Ab
- Known as:
- PDPK1 pTyr9 (anti-) Antibody
- Catalog number:
- 1488109
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- PDPK1 pTyr9 antibody
Related genes to: PDPK1 pTyr9 antibody Ab
- Gene:
- PDPK1 NIH gene
- Name:
- 3-phosphoinositide dependent protein kinase 1
- Previous symbol:
- -
- Synonyms:
- PDK1
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2015-08-25
Related products to: PDPK1 pTyr9 antibody Ab
Related articles to: PDPK1 pTyr9 antibody Ab
- Dysregulation of signaling pathways governing cell growth, survival, metabolism, angiogenesis, invasion, metastasis, and therapeutic response drives cancer progression. The AGC family of kinases, such as AKT, S6K, SGK, RSK, and PKC, is important for downstream signaling. The 3-phosphoinositide-dependent protein kinase-1 protein (PDK1), encoded by the PDPK1 gene, phosphorylates activation-loop residues in these kinases and links phosphoinositide signaling to cellular growth, survival, metabolism, and transformation. The structure, regulation, cancer-associated functions, and therapeutic targeting of PDK1 are critically reviewed, with a focus on the pleckstrin homology domain, PIF pocket-mediated substrate docking, the kinase domain, and reported non-catalytic interactions. Experimental results from breast, lung, gastric, liver, hematological, and melanoma models suggest that dysregulated PDK1 signaling can increase the output of the PI3K-AKT-mTOR pathway, invasion, metabolic adaptation, and resistance to specific hormonal, chemotherapeutic, and targeted therapies. In some preclinical models, genetic suppression of PDK1 using siRNA, shRNA, or CRISPR-based methods has been shown to slow tumor cell growth and restore drug sensitivity. However, PDK1 remains an unvalidated therapeutic target in the clinic. There is no selective PDK1 inhibitor that has been clinically approved, and most pharmacological candidates are based on biochemical and cellular data. There is limited genetic evidence and in vivo evidence, and no validated clinical evidence specific to PDK1. Emerging PIF-pocket ligands, dual-site inhibitors, allosteric modulators, and protein-degradation strategies are therefore investigational strategies that need to be improved in terms of selectivity, pharmacokinetic characterization, tumor-context validation, and biomarker-guided evaluation. - Source: PubMed
Publication date: 2026/09/10
Honnasiddappa Darshana BallagereRamar MohankumarBiju TincySajjan MallikarjunVenkatesh ChidanandaMahadeva Nayan KumarKunjiappan SelvarajAmmunje Damodar NayakPavadai Parasuraman - Oxidative stress-mediated impairment of osteoblast function is a critical pathological basis for the development and progression of various bone metabolic diseases. BicC family RNA binding protein 1 (BICC1) plays important roles in osteoblast function, however, the underlying mechanism remains unclear. This study aimed to investigate the protective role of BICC1 in oxidative stress-induced osteogenic injury and the underlying mechanism. An oxidative injury model was established in MC3T3-E1 cells using 300 µM hydrogen peroxide (HO). Bicc1 over-expressing lentivirus and the pyruvate dehydrogenase kinase isozyme (PDK) inhibitor dichloroacetate (DCA) were used for intervention. The osteoblast differentiation and mitochondrial membrane potential and apoptosis were measured by biochemical analysis and Alizarin Red S staining. RT-qPCR and Western blot were used to detect mRNA and protein levels of key molecules. RNA sequencing was performed to identify core targets and signaling pathways. H₂O₂ treatment significantly suppressed MC3T3-E1 cell viability and osteogenic differentiation, enhanced apoptosis, and up-regulated PDK1 expression as well as pyruvate dehydrogenase complex (PDH) phosphorylation. Bicc1 over-expression markedly alleviated H₂O₂-induced mitochondrial dysfunction and apoptosis, restored osteogenic differentiation, and inhibited the activation of the PDK1/PDH axis. Transcriptomic analysis showed that PDK1 was a key target molecule in Bicc1-regulated apoptosis and oxidative stress responses. Inhibition of PDK1 recapitulates the protective effect of BICC1 to oxidative stress injury in MC3T3-E1 cells. Bicc1 attenuates oxidative stress injury and promotes osteogenic differentiation in MC3T3-E1 cells, and may serve as a potential therapeutic target for osteoporosis. - Source: PubMed
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