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anti-Human MCU Antikörper:
anti-Mouse (Murine) MCU Antikörper:
anti-Rat (Rattus) MCU Antikörper:
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Human Polyclonal MCU Primary Antibody für ICC, IF - ABIN4288500
Baughman, Perocchi, Girgis, Plovanich, Belcher-Timme, Sancak, Bao, Strittmatter, Goldberger, Bogorad, Koteliansky, Mootha: Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter. in Nature 2011
Show all 8 Pubmed References
MICU1 imparts the mitochondrial uniporter with the ability to discriminate between Ca(2+) and Mn(2+).
Mitochondrial Ca(2+) uptake is controlled by protein arginine methyl transferase 1 that asymmetrically methylates MICU1, resulting in decreased Ca(2+) sensitivity. UCP2/3 normalize Ca(2+) sensitivity of methylated MICU1 and, thus, re-establish mitochondrial Ca(2+) uptake activity.
VDAC1 allows Ca(2+) access to the MCU, facilitating transport of Ca(2+) to the matrix, and also from the IMS to the cytosol. Intra-mitochondrial Ca(2+) controls energy production and metabolism by modulating critical enzymes in the tricarboxylic acid (TCA) cycle and fatty acid oxidation.
MICU2 restricts spatial crosstalk between InsP3R and MCU channels by regulating threshold and gain of MICU1-mediated inhibition and activation of MCU.
The results highlight the dynamic nature of uniporter subunit assembly, which must be tightly regulated to ensure proper mitochondrial responses to intracellular Ca(2+) signals.
MCU expression returned to physiological levels in visceral adipose tissue of patients after weight loss by bariatric surgery. Altered mitochondrial calcium flux in fat cells may play a role in obesity and diabetes and may be associated with the differential metabolic profiles of visceral and subcutaneous adipose tissue.
Mitochondrial calcium uniporter plays an important role in hyperglycaemia-induced endothelial cell dysfunction.
The studies findings in aging human skeletal muscle confirm the data obtained in mice and propose mitochondrial calcium uniporter and mitochondria-related proteins as potential pharmacological targets to counteract age-related muscle loss.
decreased MCU expression in hypertensive with mutation cells contributed to dysregulated Ca(2+) uptake into the mitochondria
The molecular structure and regulation of the MCU complex in addition to its pathophysiological role are discussed with particular attention to striated muscle tissues. Review.
High MCU expression is associated with metastasis in hepatocellular carcinoma.
Here, the authors determine the transmembrane orientation of EMRE, and show that its known MCU-activating function is mediated by the interaction of transmembrane helices from both proteins.
It has been shown that the propagation of the TRPV1-induced cytosolic calcium and sodium fluxes into mitochondria is dependent on coordinated activity of NCLX and MCU.
Regulation of mitochondrial Ca(2+) suggests that MCU may play a pivotal role in the development of fibrosis and could potentially be a therapeutic target for pulmonary fibrosis.
MCU downregulation hampered cell motility and invasiveness and reduced tumor growth, lymph node infiltration, and lung metastasis in triple-negative breast cancer xenografts. In MCU-silenced cells, production of mitochondrial reactive oxygen species (mROS) is blunted and expression of the hypoxia-inducible factor-1alpha (HIF-1alpha) is reduced, suggesting a signaling role for mROS and HIF-1alpha, downstream of mitochon...
Reveal a distinct functional role for Cys-97 in mitochondrial reactive oxygen species sensing and regulation of MCU activity.
Study indicates that inhibition of mitochondrial calcium uniporter can inhibit excessive mitophagy and protect the neurocytes from ischemia/reperfusion injury.
Our experiments provide novel details about how MCU/EMRE is regulated by MICU1 and an original approach to investigate MCU/EMRE activation in intact cells.
Data suggest that MCU regulator (EMRE) might be a structural factor for opening of the mitochondrial calcium uniporter (MCU)-forming pore.
results suggest that N terminal domain of MCU is essential for the modulation of MCU function, although it does not affect the uniplex formation
the endothelial barrier was preserved in respiratory epithelium isolated from MCU-/- mice after exposure to IL-13. In the ovalbumin-model of allergic airway disease, MCU deficiency resulted in decreased apoptosis within the large airway epithelial cells. Concordantly, expression of the tight junction protein ZO-1 was preserved, indicative of maintenance of epithelial barrier function
Results suggest that inhibition of MCU attenuates Abeta-induced mcroglial apoptosis, and that it does so through modulation of reactive oxygen species-mediated endoplasmic reticulum stress. Understanding the apparent links between endoplasmic reticulum stress, oxidative stress and MCU could lead to the development of therapeutic strategies targeting Abeta-mediated microglial death.
These data indicate that Ca(2+) uptake via mitochondrial uniporter contributes to palmitic acid-induced apoptosis in mouse podocytes.
a possible role for tissue-specific stoichiometry between the Ca(2+)-sensing regulators (MICUs) and pore unit (MCU) of the uniporter, was investigated.
MCUR1 binds to MCU and EMRE and function as a scaffold factor.
MCU and EMRE proteins were mainly targeting to the IMM-outer mitochondrial membrane.
The m-AAA protease associated with neurodegeneration limits MCU activity in mitochondria.
Data show that the serine/threonine kinase LKB1 regulates mitochondrial calcium uniporter (MCU)-expression, mitochondria-dependent Ca2+ clearance, and thereby, presynaptic release properties.
the Mcu-regulating Micu gene family profile differs substantially between neurons and astrocytes, while expression of Mcu itself is markedly different between CA3 and CA1 regions in the adult hippocampus.
Absence of MCU expression does not affect basal cardiac function at either 12 or 20months of age in knockout mice.
MCU is required to match energetics with contractile demand during stress. Deletion of Mcu protects against myocardial IR injury.
Mice lacking MCU in the heart show no pathology. MCU selectively mediates acute mitochondria Ca2+ loading to augment ATP synthesis.
MCU is necessary for complete physiological heart rate acceleration
MCU-VDAC1 complex regulates mitochondrial Ca(2+) uptake and oxidative stress-induced apoptosis
Chromatin immunoprecipitation and promoter reporter analyses revealed that the Ca2+ -regulated transcription factor CREB (cyclic adenosine monophosphate response element-binding protein) directly bound the MCU promoter and stimulated expression.
chronic myocardial MCU inhibition leads to previously unanticipated compensatory changes.
Tetrodotoxin-sensitive mitochondrial Ca(2+) influx was largely blocked by knockdown of MCU expression.
This gene encodes a calcium transporter that localizes to the mitochondrial inner membrane. The encoded protein interacts with mitochondrial calcium uptake 1. Alternative splicing results in multiple transcript variants.
calcium uniporter protein, mitochondrial
, coiled-coil domain-containing protein 109A
, coiled-coil domain containing 109A