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The substrate transported is not yet known. Additionally we are shipping MTCH2 Antibodies (51) and many more products for this protein.
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MTCH2 and cardiolipin participate in the recruitment and integration of tBID into the mitochondrial outer membrane.
The BID (show BID Proteins)-MTCH2 axis regulates the differentiation/apoptosis of stem cells and mitochondrial metabolism. (Review)
Data indicate that Mtch2 accelerated conformational change in membrane-bound tBid (Bid (show BID Proteins)) enables it to activate Bax (show BAX Proteins).
Compares and contrasts all the known human SLC25A (show SLC25A25 Proteins)* genes and includes functional information.
Results imply a regulatory role for TMEM18 (show TMM18 Proteins), BDNF (show BDNF Proteins), MTCH2 and NEGR1 (show NEGR1 Proteins) in adipocyte differentiation and biology. In addition, we show a variation of MAF (show MAF Proteins) expression during adipogenesis, while NPC1 (show NPC1 Proteins), PTER (show PTER Proteins) and SH2B1 (show SH2B1 Proteins) were not regulated.
Our study supports earlier reports of SH2B1 (show SH2B1 Proteins) to be of importance in insulin (show INS Proteins) sensitivity and, in addition, suggests potential roles of NEGR1 (show NEGR1 Proteins) and MTCH2.
Molecular basis of the interaction between proapoptotic truncated BID (show BID Proteins) (tBID) protein and mitochondrial carrier homologue 2 (MTCH2) protein
Gene-treatment interactions were observed for short-term weight loss. (MTCH2 rs10838738, Plifestyle*SNP = 0.022)
MTCH2 may play a role in cellular processes underlying obesity
MTCH2 rs 10838738 is associated with higher body mass index.
The findings indicate an essential role for mtch2 during organ development and adipogenesis in vivo.
Results show that Mimp/Mtch2 overexpression alters lipid metabolism and may play a role in the onset of obesity and development of insulin (show INS Proteins) resistance.
MTCH2 is a conserved regulator of lipid homeostasis. MTCH2 was found to be both required and sufficient for lipid homeostasis shifts, suggesting that pharmacological inhibition of MTCH2 could be therapeutic for treatment of obesity and related disorders. MTCH2 could influence lipid homeostasis through inhibition of ESR1 (show ESR1 Proteins) activity.
Loss of MTCH2 increases muscle metabolism, energy expenditure, heart function, and protects from diet-induced obesity.
Loss of Mtch2 increases mitochondrial OXPHOS, triggering HSC (show FUT1 Proteins) entry into cycle. Elevated OXPHOS is accompanied by an increase in mitochondrial size, increase in ATP and ROS (show ROS1 Proteins) levels, and protection from irradiation-induced apoptosis.
The substrate transported is not yet known. Induces mitochondrial depolarization (By similarity).
, met-induced mitochondrial protein
, mitochondrial carrier homolog 2
, solute carrier family 25, member 50