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MCU encodes a calcium transporter that localizes to the mitochondrial inner membrane. Additionally we are shipping MCU Proteins (6) and MCU Antibodies (3) and many more products for this protein.
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Our experiments provide novel details about how MCU/EMRE is regulated by MICU1 (show MICU1 ELISA Kits) 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
MCU-VDAC1 (show VDAC1 ELISA Kits) complex regulates mitochondrial Ca(2 (show CA2 ELISA Kits)+) uptake and oxidative stress-induced (show SQSTM1 ELISA Kits) apoptosis
Loss of heterozygosity of MCU gene on chromosome 10q is associated with pancreatic cancer.
Studies indicate the existence of an inner mitochondrial protein (show COX6B2 ELISA Kits) termed the mitochondrial calcium uniporter for calcium transport.
analyses establish that MCU encodes the pore-forming subunit of the uniporter channel
MCU plays a critical role in breast cancer cell migration by regulating store-operated Ca(2 (show CA2 ELISA Kits)) entry.
SLC25A23 (show SLC25A24 ELISA Kits) augments mitochondrial Ca(2 (show CA2 ELISA Kits)) uptake, interacts with MCU, and induces oxidative stress-mediated cell death.
We review not only the biochemical identities and structures of the proteins required for mitochondrial Ca2 (show CA2 ELISA Kits)+ uptake but also their implications in different physiopathological contexts. [review]
the Mcu-regulating Micu gene family profile differs substantially between neurons and astrocytes, while expression of Mcu itself is markedly different between CA3 (show CA3 ELISA Kits) and CA1 (show CA1 ELISA Kits) 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 (show CA2 ELISA Kits)+ loading to augment ATP synthesis.
MCU is necessary for complete physiological heart rate acceleration
Chromatin immunoprecipitation and promoter reporter analyses revealed that the Ca2 (show CA2 ELISA Kits)+ -regulated transcription factor CREB (show CREB1 ELISA Kits) (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 (show CA2 ELISA Kits)+) influx was largely blocked by knockdown of MCU expression.
Characterization of MCU deficient mice indicates that acute alterations in mitochondrial matrix calcium can regulate mammalian physiology.
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