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may be involved in apoptosis of neuronal cells. Additionally we are shipping Brain Protein 44-Like Antibodies (44) and Brain Protein 44-Like Proteins (4) and many more products for this protein.
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Hypoxia induces lactate secretion and glycolytic efflux by downregulating MPC1/MPC2 levels in HUVEC cells.
Low MPC1 expression is associated with epithelial-mesenchymal transition in cholangiocarcinoma.
Levels of lactate and mitochondrial pyruvate carrier (MPC1) mRNA were determined to scrutinize the prevalence of aerobic glycolysis..MT-RNR2 plays its anti-apoptotic role partly by avoiding deploying energy from complete oxidation of organic compounds to inorganic wastes. Thus MT-RNR2 can potentially serve as a new biomarker in the diagnosis of bladder carcinoma especially that it is present in blood circulation
Low MPC1 expression is associated with prostate cancer.
Utilizing zebrafish to examine the genetic relationship between MPC1 and Adenomatous polyposis coli (APC (show APC ELISA Kits)), a key tumor suppressor in colorectal cancer, the authors found that apc (show APC ELISA Kits) controls the levels of mpc1 and that knock down of mpc1 recapitulates phenotypes of impaired apc (show APC ELISA Kits) function including failed intestinal differentiation.
Results indicate mitochondrial pyruvate transporter (MPC) to be the key regulatory junction perturbed by virulent strains of Mycobacterium tuberculosis leading to alteration of mitochondrial metabolic flux and regulation of acetyl-CoA (show LPCAT2 ELISA Kits) formation.
GTPBP3 (show GTPBP3 ELISA Kits) plays a role in the regulation of MCP1 (show CCL2 ELISA Kits) protein through AMPK (show PRKAA1 ELISA Kits) signaling.
Tumor cells expressing MPC1 and MPC2 display increased mitochondrial pyruvate oxidation, with no changes in cell growth in adherent culture.
genetic studies of 3 families with children suffering from lactic acidosis and hyperpyruvatemia revealed a causal locus that mapped to MPC1 (BRP44L) changing single amino acids that are conserved throughout eukaryotes; data demonstrate that Mpc1 and Mpc2 form an essential part of the mitochondrial pyruvate carrier
the MPC1 knockout blocks mitochondrial pyruvate uptake and OXPHOS, which results in metabolic reprogramming towards aerobic Warburg glycolysis with reduced ATP production capability.
Heterozygous MPC1 KO weakens fertility and influences the metabolism of glucose and fatty acid and bodyweight in mice.
This study suggests that inhibition of MPC1 activity can boost fatty acid oxidation to provide sufficient energy to the body.
Our study indicates that MPC1 and MPC2 expressions are of prognostic values in PCAs and that positive expression of MPC1 or MPC2 is a predictor of favorable outcome.
Results show that Mpc1 is required for mammalian embryonic development and efficient pyruvate metabolism.
This resulted in embryonic lethality at around E13.5. Mouse embryonic fibroblasts (MEFs) derived from mutant mice displayed defective pyruvate-driven respiration as well as perturbed metabolic profiles, and both defects could be restored by reexpression of MPC1.
Oxidative glutaminolysis supports the TCA cycle in mouse cells lacking MPC1/2.
The protein encoded by this gene is part of an MPC1/MPC2 heterodimer that is responsible for transporting pyruvate into mitochondria. The encoded protein is found in the inner mitochondrial membrane. Defects in this gene are a cause of mitochondrial pyruvate carrier deficiency. Several transcript variants, some protein coding and one non-protein coding, have been found for this gene.
brain protein 44-like
, brain protein 44-like protein a
, brain protein 44-like protein b
, brain protein 44-like protein
, putative brain protein 44-like variant 2
, mitochondrial pyruvate carrier 1
, HSPC040 protein
, apoptosis-regulating basic protein