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The substrate transported is not yet known. Zusätzlich bieten wir Ihnen MTCH2 Antikörper (59) und viele weitere Produktgruppen zu diesem Protein an.
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study identified Cav1 (zeige CAV1 Proteine) and MTCH2 as the molecular targets of DHA and revealed a new link between the upstream Cav1 (zeige CAV1 Proteine)/MTCH2 upregulation and the downstream activation of the cell death pathway involved in the DHA-mediated inhibition of cell viability.
MTCH2 and cardiolipin participate in the recruitment and integration of tBID into the mitochondrial outer membrane.
The BID (zeige BID Proteine)-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 (zeige BID Proteine)) enables it to activate Bax (zeige BAX Proteine).
Compares and contrasts all the known human SLC25A (zeige SLC25A25 Proteine)* genes and includes functional information.
Results imply a regulatory role for TMEM18 (zeige TMM18 Proteine), BDNF (zeige BDNF Proteine), MTCH2 and NEGR1 (zeige NEGR1 Proteine) in adipocyte differentiation and biology. In addition, we show a variation of MAF (zeige MAF Proteine) expression during adipogenesis, while NPC1 (zeige NPC1 Proteine), PTER (zeige PTER Proteine) and SH2B1 (zeige SH2B1 Proteine) were not regulated.
Our study supports earlier reports of SH2B1 (zeige SH2B1 Proteine) to be of importance in insulin (zeige INS Proteine) sensitivity and, in addition, suggests potential roles of NEGR1 (zeige NEGR1 Proteine) and MTCH2.
Molecular basis of the interaction between proapoptotic truncated BID (zeige BID Proteine) (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
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 (zeige INS Proteine) 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 (zeige ESR1 Proteine) 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 (zeige FUT1 Proteine) entry into cycle. Elevated OXPHOS is accompanied by an increase in mitochondrial size, increase in ATP and ROS (zeige ROS1 Proteine) 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