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抗Mouse (Murine) PDK1 抗体:
抗Human PDK1 抗体:
Here, the authors show that loss of Fxn (显示 FXN 抗体) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (显示 PDPK1 抗体)/Mef2 (显示 MEF2C 抗体) pathway, indicating that the mechanism is evolutionarily conserved.
PDK1 (显示 PDPK1 抗体) has broad effects in hematopoiesis and is a critical factor for engraftment of both hematopoietic stem cells and multipotent progenitors upon transplantation to recipient mice.
our results offer significant insight into how PIK3CA (显示 PIK3CA 抗体) overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K/PDK1 (显示 PDPK1 抗体) and TGFb (显示 TGFB1 抗体) signaling in advanced HNSCC patients with PIK3CA (显示 PIK3CA 抗体) amplification
PTEN (显示 PTEN 抗体) is required for stabilization of planar cell packing in the neural plate and for the formation of stable apical-basal microtubule arrays, while PDPK1 (显示 PDPK1 抗体) is required for stabilization of apical junctions during epithelial morphogenesis.
results thus reveal an essential role for the PDK1 (显示 PDPK1 抗体)-Akt (显示 AKT1 抗体) pathway in the regulation of a key step of neuronal migration.
PDK1 (显示 PDPK1 抗体) plays a pivotal role in regulating cardiac function and tumor metastasis by interfering with microenvironment.
Our data suggest that two arms of the glucose metabolism synergistically regulate the differential activation of macrophages. Our findings also highlight the central role of PDK1 (显示 PDPK1 抗体) in this event via controlling glycolysis and glucose oxidation.
PDHK1 is expressed in Th17 cells, but not Th1 (显示 HAND1 抗体) cells, and at low levels in Tregs, and inhibition or knockdown of PDHK1 selectively suppressed Th17 cells and increased Tregs.
The tyrosine phosphorylation enhances PDHK1 kinase activity by promoting ATP and PDC (显示 PDC 抗体) binding.
Pdk1 (显示 PDPK1 抗体) enzyme is critical in conserving mitochondrial function by diverting metabolic intermediates to glycolysis
The pyruvate dehydrogenase (显示 PDP 抗体) kinases (PDKs) PDK1 and PDK3 (显示 PDK3 抗体) are direct targets of KDM4A (显示 KDM4A 抗体) and E2F1 (显示 E2F1 抗体) and modulate the switch between glycolytic metabolism and mitochondrial oxidation.
Ribociclib, in combination with GSK2334470 or the PI3Kalpha (显示 PIK3CA 抗体) inhibitor alpelisib, decreased xenograft tumor growth more potently than each drug alone. Taken together, our results highlight a role for the PI3K (显示 PIK3CA 抗体)-PDK1 signaling pathway in mediating acquired resistance to CDK4/6 (显示 CDK4 抗体) inhibitors.
dicumarol potently inhibited the kinase activity of PDK1, shifted the glucose metabolism from aerobic glycolysis to oxidative phosphorylation, generated a higher level of reactive oxygen species (ROS (显示 ROS1 抗体)), attenuated the mitochondrial membrane potential (MMP), induced apoptosis, and reduced cell viability in vitro.
our results offer significant insight into how PIK3CA (显示 PIK3CA 抗体) overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K (显示 PIK3CA 抗体)/PDK1 and TGFb (显示 TGFB1 抗体) signaling in advanced HNSCC patients with PIK3CA (显示 PIK3CA 抗体) amplification
miR (显示 MLXIP 抗体)-379 could function as a tumour-suppressing miRNA via targeting PDK1 in osteosarcoma.
These results also suggest that inhibition of HIF-1a (显示 HIF1A 抗体) with 2-MeOE2 sensitizes radioresistant melanoma cells 435R to X-ray irradiation through targeting the glycolysis that is regulated by PDK1
PDK1 is frequently upregulated in primary nasopharyngeal carcinoma and may serve as a prognostic marker.
A new function for PDK1 in metabolic reprogramming, which could be used to indicate the prognosis of Non small cell lung cancer and provide targeted therapeutic strategy for clinical treatment.
Our results demonstrated that down-regulation of SDHB (显示 SDHB 抗体) and up-regulation of PDK1 may be novel biomarkers for predicting advanced tumor progression and unfavorable prognosis in recurrent nasopharyngeal carcinoma patients
n the conditon of miR (显示 MLXIP 抗体)- 128b over-expression, we also observed spontaneous inactivation of the Akt (显示 AKT1 抗体)/NF-kappaB (显示 NFKB1 抗体) signalling, implying PDK1 was a potential regulator of this pathway. In conclusion, our study shed some novel light on miR (显示 MLXIP 抗体)-128b-PDK1/Akt (显示 AKT1 抗体)/NF-kappaB (显示 NFKB1 抗体) axis onGastric cancer (GC) progression
Dephosphorylation of PDK1 may be a molecular switch for enhancement of protein tyrosine phosphorylation and flagellar hyperactivation in boar spermatozoa.
Pyruvate dehydrogenase (PDH) is a mitochondrial multienzyme complex that catalyzes the oxidative decarboxylation of pyruvate and is one of the major enzymes responsible for the regulation of homeostasis of carbohydrate fuels in mammals. The enzymatic activity is regulated by a phosphorylation/dephosphorylation cycle. Phosphorylation of PDH by a specific pyruvate dehydrogenase kinase (PDK) results in inactivation.
pyruvate dehydrogenase kinase, isoenzyme 1
, pyruvate dehydrogenase kinase, isozyme 1
, pyruvate dehydrogenase [lipoamide] kinase isozyme 1, mitochondrial-like
, PDH kinase 1
, [Pyruvate dehydrogenase [lipoamide]] kinase isozyme 1, mitochondrial
, mitochondrial pyruvate dehydrogenase, lipoamide, kinase isoenzyme 1
, PDK p48
, pyruvate dehydrogenase kinase 1