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Here, the authors show that loss of Fxn (show FXN ELISA Kits) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (show PDPK1 ELISA Kits)/Mef2 (show MEF2C ELISA Kits) pathway, indicating that the mechanism is evolutionarily conserved.
PDK1 (show PDPK1 ELISA Kits) 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 (show PIK3CA ELISA Kits) overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K/PDK1 (show PDPK1 ELISA Kits) and TGFb (show TGFB1 ELISA Kits) signaling in advanced HNSCC patients with PIK3CA (show PIK3CA ELISA Kits) amplification
PTEN is required for stabilization of planar cell packing in the neural plate and for the formation of stable apical-basal microtubule arrays, while PDPK1 (show PDPK1 ELISA Kits) is required for stabilization of apical junctions during epithelial morphogenesis.
results thus reveal an essential role for the PDK1 (show PDPK1 ELISA Kits)-Akt (show AKT1 ELISA Kits) pathway in the regulation of a key step of neuronal migration.
PDK1 (show PDPK1 ELISA Kits) 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 (show PDPK1 ELISA Kits) in this event via controlling glycolysis and glucose oxidation.
PDHK1 is expressed in Th17 cells, but not Th1 (show HAND1 ELISA Kits) 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 (show PDC ELISA Kits) binding.
Pdk1 (show PDPK1 ELISA Kits) enzyme is critical in conserving mitochondrial function by diverting metabolic intermediates to glycolysis
The pyruvate dehydrogenase (show PDP ELISA Kits) kinases (PDKs) PDK1 and PDK3 (show PDK3 ELISA Kits) are direct targets of KDM4A (show KDM4A ELISA Kits) and E2F1 (show E2F1 ELISA Kits) and modulate the switch between glycolytic metabolism and mitochondrial oxidation.
Ribociclib, in combination with GSK2334470 or the PI3Kalpha (show PIK3CA ELISA Kits) inhibitor alpelisib, decreased xenograft tumor growth more potently than each drug alone. Taken together, our results highlight a role for the PI3K (show PIK3CA ELISA Kits)-PDK1 signaling pathway in mediating acquired resistance to CDK4/6 (show CDK4 ELISA Kits) 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 (show ROS1 ELISA Kits)), attenuated the mitochondrial membrane potential (MMP), induced apoptosis, and reduced cell viability in vitro.
our results offer significant insight into how PIK3CA (show PIK3CA ELISA Kits) overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K (show PIK3CA ELISA Kits)/PDK1 and TGFb (show TGFB1 ELISA Kits) signaling in advanced HNSCC patients with PIK3CA (show PIK3CA ELISA Kits) amplification
miR (show MLXIP ELISA Kits)-379 could function as a tumour-suppressing miRNA via targeting PDK1 in osteosarcoma.
These results also suggest that inhibition of HIF-1a (show HIF1A ELISA Kits) 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 (show SDHB ELISA Kits) 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 (show MLXIP ELISA Kits)- 128b over-expression, we also observed spontaneous inactivation of the Akt (show AKT1 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) signalling, implying PDK1 was a potential regulator of this pathway. In conclusion, our study shed some novel light on miR (show MLXIP ELISA Kits)-128b-PDK1/Akt (show AKT1 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) 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