PDK1
- Known as:
- PDK1
- Catalog number:
- 000581A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PDK1
Related genes to: PDK1
- Gene:
- PDK1 NIH gene
- Name:
- pyruvate dehydrogenase kinase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-14
- Date modifiied:
- 2016-01-06
- 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: PDK1
3-phosphoinositide-dependent protein kinase 1,Homo sapiens,hPDK1,Human,PDK1,PDPK13-phosphoinositide-dependent protein kinase 1,Mouse,mPDK1,Mus musculus,Pdk1,Pdpk13-phosphoinositide-dependent protein kinase 1,Pdk1,Pdpk1,PkB kinase,Protein kinase B kinase,Rat,Rattus norvegicus3_Phosphoinositide Dependent Protein Kinase_1 (PDK1&_65292;active)3_phosphoinositide dependent protein kinase_1 [S241] (PDK1) polyclonal antibodyActive PDK1Active PDK1Active PDK1, recombinant human proteinAnti- PDK1 (Ab-241) AntibodyAnti- PDK1 (Ab-241) AntibodyAnti- PDK1 (Phospho-Ser241) AntibodyAnti- PDK1 (Phospho-Ser241) Antibodyanti-PDK1Anti-PDK1 produced in rabbit Antibodyanti-PDK1 (4A11) Related articles to: PDK1
- Semaphorin 7A (SEMA7A), a membrane-anchored glycoprotein involved in immune and vascular signalling, has been implicated in cardiovascular diseases. However, its role in the development of abdominal aortic aneurysm (AAA) has not been defined. In this study, we investigated the role of SEMA7A in AAA progression and the underlying mechanisms. - Source: PubMed
Li FengchanZhu ZhenTang FanDu YunLyu JiaxinWu LiliNi HaofuWang YingRen LijieLu QiongyuLiu HuihuiHong LeiWang HongjieTang ChaojunZhu Li - Metabolomics analyses suggest abnormal purine metabolism during the development of osteoporosis. This study aimed to investigate the role of purine metabolism-related genes in osteoporosis. - Source: PubMed
Publication date: 2025/11/07
Zeng YuqingHu JintaoLu JianweiZhu Yunyun - Deubiquitinating enzymes are important regulators of cancer progression. We explored the role and regulatory mechanisms of the deubiquitinating enzyme ubiquitin-specific protease 22 (USP22) in neuroblastoma (NB). USP22 expression was upregulated in NB patient tissue samples and its expression correlated with their overall survival. Knockdown of USP22 in NB cell lines suppressed cell proliferation, invasion and glycolysis, and enhanced apoptosis. A coimmunoprecipitation assay identified a relationship between USP22 and 3-phosphoinositide-dependent protein kinase 1 (PDK1). USP22 stabilized PDK1 expression via deubiquitination; PDK1 overexpression reversed the effects of USP22 knockdown on the malignant behaviors of NB cells. Dual-luciferase reporter assay and RNA immunoprecipitation were utilized to clarify the relationship between Yin Yang-1 (YY1) and USP22. Yin Yang-1 regulated PDK1 expression via promoting USP22 transcription. USP22 knockdown in a xenograft assay also inhibited tumor growth via regulating PDK1. Taken together, these results indicate that USP22 regulated by YY1 plays a promotional role in NB progression by mediating the deubiquitination of PDK1. - Source: PubMed
Zhang DiGu TingCao GengfeiHu ChunweiYang Huiting - Macrophage M2 polarization plays a critical role in the progression of endometriosis (EMS), and glycolysis has emerged as a potential therapeutic target. This study aimed to investigate the interplay between glycolytic signaling and macrophage M2 polarization in EMS. - Source: PubMed
Publication date: 2025/06/04
Li HanChai Xiaoshan - The Alzheimer's disease (AD)-affected brain is known to be deficient in the utilization of glucose, its main energy substrate, and systemic diabetes is a significant risk factor for AD. In the course of biochemical and molecular investigations into this puzzling relationship, it has been shown that resistance to insulin action is a prominent feature of early stages of AD in the brain, thereby contributing to an energy failure state and a decline in synaptic function. In one AD-like cellular model, we found that β-amyloid (Aβ) accumulation inhibited insulin signaling and cell viability through an alteration of the PI3K/PDK-1/Akt signal pathway, an effect overcome by mTORC2 stimulation. A PDK-1 allosteric agonist, PS48, as well as newly synthesized analogs, were also found to reverse the metabolic defects caused by intracellular Aβ42 accumulation. In vivo, we previously showed that oral dosing of PS48 significantly improves learning and memory in APP/PS1 transgenic mice. Herein, we present evidence using unbiased immunohistological quantification and Western blot analyses demonstrating that ingested PS48 crosses into brain tissue where it targeted Akt and GSK3-β activities. Beneficial effects on neuronal number and Tau phosphorylation were found. Not unexpectedly, Aβ levels remained unchanged. These results support a path toward a future therapeutic trial of this untested strategy and agent in humans. - Source: PubMed
Publication date: 2025/04/08
Querfurth Henry WLemere CynthiaCiola JasonHavas DanielXia WeimingLee Han Kyu