Ask about this productRelated genes to: PDK1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: PDK1 Blocking Peptide
- 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
Publication date: 2026/09/08
Liu ZhongshuangChen AijieLi BaoxuLi ShibinHuang WeibinXie QiTao FuchengSu LeyaoZhu KairanLiu QiMa Lin - Diabetic patients often experience poor outcomes due to vascular diseases, yet the current treatments have not been effective. Physical activity is able to improve health conditions in diabetic patients. However, the exact mechanisms are not fully understood. Forkhead Box O1 (FoxO1), a key modulator of cellular metabolism, has been depicted to trigger diabetic vascular remodeling in our previous study. It is reported that improvement of insulin resistance through aerobic exercise is closely linked to the activity of 3-phosphoinositide-dependent kinase 1 (PDK1), which acts as an important upstream component of the FoxO1 signaling pathway. Here, we aimed to explore whether aerobic exercise could ameliorate diabetes-induced vascular remodeling and discuss the role of the PDK1/FoxO1 axis in this process. The type I diabetes mouse models were established by intraperitoneal injection of streptozotocin (STZ) for three months. The structure modeling of the carotid artery was analyzed by immunofluorescence analysis. The expression profiles of PDK1, FoxO1, inflammatory markers (NLRP3, VCAM-1, CCR2, and NF-κB), and contractive/proliferative biomarkers of smooth muscle cells (α-SMA/MMP-2, MMP-9) in both artery tissues and cells were evaluated by immunofluorescence and western blotting analyses. Unpaired t-test and one-way ANOVA were utilized to compare the groups. PDK1 expression in carotid tissues was decreased in diabetic mice after 3 months of STZ induction, whereas the FoxO1 level was upregulated. The diabetic mice exhibited adverse structural changes in the carotid arteries, including thicker walls and a reduced size of the inner cavity. Moreover, these vasculopathies were accompanied by increased levels of inflammatory markers such as NLRP3 and NF-κB. Importantly, these alterations were reversed by 3-month aerobic exercise. Collectively, this study indicates that aerobic exercise plays a protective function in the diseased blood vessels of diabetic mice through activating the PDK1/FoxO1 pathway. Therefore, targeting the PDK1/FoxO1 signaling axis could become a promising option for the treatment of diabetes-associated cardiovascular diseases. - Source: PubMed
Xie XiangZhang ZihanYang XumeiChu Man - Despite being a well-established oncogenic regulator of metabolism promoting aerobic glycolysis, the pan-cancer prognostic value of PDK1, along with its immunomodulatory activity, is still poorly understood. In this research, an integrated multi-omics analysis was used to describe the expression of PDK1 and its prognostic role and immunomodulatory activity in different types of cancers, but specifically in kidney renal clear cell carcinoma (KIRC). It was found that PDK1 was overexpressed in various types of cancers, in which it always presented poor prognostic factors. Low PDK1 levels of tumors preserved an immunologically active microenvironment, and high PDK1 expression was recognized to be sensitive to chemotherapy and targeted agents. In KIRC, in particular, high PDK1 levels were linked to high TIL and PD-L1, which supports the idea that PDK1 is a combined immunological and prognostic biomarker. These results define the multifactorial functions of PDK1 in tumorigenesis and immunoregulation, which opens the path to the creation of PDK1-targeted therapies in clinical oncology. - Source: PubMed
Publication date: 2026/02/28
Duan ShuangshuangZhang MengmengSun MiaoAbudusaimaiti GulinaizaierZhang LijunLiu Huibin - LCZ696 (sacubitril/valsartan) can attenuate early cardiac remodelling of heart failure (HF), although it is less effective in severe remodelling. Surgical ventricular reconstruction (SVR) is used to treat refractory HF with large ventricular aneurysms (LVA), but residual remodelling limits the long-term survival. It is unknown whether LCZ696 can mitigate residual remodelling. - Source: PubMed
Publication date: 2026/01/12
Yan JunyuLi DantongQiu XuetingTan NingYang Dahao - 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