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The substrate transported is not yet known. Additionally we are shipping MTCH2 Proteins (4) and many more products for this protein.
Showing 10 out of 63 products:
Human Polyclonal MTCH2 Primary Antibody for IHC (p), WB - ABIN651683
Steffen, Vashisht, Wan, Jen, Claypool, Wohlschlegel, Koehler: Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria. in Molecular biology of the cell 2017
study identified Cav1 and MTCH2 as the molecular targets of DHA and revealed a new link between the upstream Cav1/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-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) enables it to activate Bax.
Compares and contrasts all the known human SLC25A* genes and includes functional information.
Results imply a regulatory role for TMEM18, BDNF, MTCH2 and NEGR1 in adipocyte differentiation and biology. In addition, we show a variation of MAF expression during adipogenesis, while NPC1, PTER and SH2B1 were not regulated.
Our study supports earlier reports of SH2B1 to be of importance in insulin sensitivity and, in addition, suggests potential roles of NEGR1 and MTCH2.
Molecular basis of the interaction between proapoptotic truncated BID (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.
Mtch2 is a mitochondrial target of tBID and possibly participates in the mitochondrial apoptotic program.
The findings indicate an essential role for mtch2 during organ development and adipogenesis in vivo.
Mitochondrial carrier homolog 2 protein (MTCH2) knockout (-/-) embryonic stem cells (ESCs) fail to elongate their mitochondria and to alter their metabolism.
MTCH2 is a critical player in neuronal cell biology, controlling mitochondria metabolism, motility and calcium buffering to regulate hippocampal-dependent cognitive functions.
Results show that Mimp/Mtch2 overexpression alters lipid metabolism and may play a role in the onset of obesity and development of insulin 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 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 entry into cycle. Elevated OXPHOS is accompanied by an increase in mitochondrial size, increase in ATP and ROS 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