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LETM1 encodes a protein that is localized to the inner mitochondrial membrane. De plus, nous expédions LETM1 Protéines (5) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 71 products:
Human Monoclonal LETM1 Primary Antibody pour IF, IHC (p) - ABIN561659
Dimmer, Navoni, Casarin, Trevisson, Endele, Winterpacht, Salviati, Scorrano: LETM1, deleted in Wolf-Hirschhorn syndrome is required for normal mitochondrial morphology and cellular viability. dans Human molecular genetics 2008
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Human Polyclonal LETM1 Primary Antibody pour ELISA, WB - ABIN517469
Mallilankaraman, Cárdenas, Doonan, Chandramoorthy, Irrinki, Golenár, Csordás, Madireddi, Yang, Müller, Miller, Kolesar, Molgó, Kaufman, Hajnóczky, Foskett, Madesh: MCUR1 is an essential component of mitochondrial Ca2+ uptake that regulates cellular metabolism. dans Nature cell biology 2012
Human Polyclonal LETM1 Primary Antibody pour ICC, IF - ABIN4330704
Kuum, Veksler, Liiv, Ventura-Clapier, Kaasik: Endoplasmic reticulum potassium-hydrogen exchanger and small conductance calcium-activated potassium channel activities are essential for ER calcium uptake in neurons and cardiomyocytes. dans Journal of cell science 2012
Data indicate a positive association between LETM1 up-regulation, YAP1 nuclear localization and high PDGFB expression.
LETM1 plays an important role in the progression of breast cancer
LETM1 protein overexpression is associated with Triple negative breast cancer progression, and may be a potential biomarker for poor prognostic evaluation of Triple negative breast cancer.
LETM1 plays an important role in the progression of head and neck squamous cell carcinoma.
Letm1 expression is decreased in patients with intractable TLE and a rat model of epilepsy. Down-regulation of Letm1 leads to increases mitochondrial swelling and decreased MT-CYB (Montrer MT-CYB Anticorps) expression, which is associated with susceptibility to seizures.
Reconstitution of LETM1 or antioxidant overexpression rescued mitochondrial Ca(2 (Montrer CA2 Anticorps)+) transport and bioenergetics
These findings identify novel cellular phenotypes in Wolf-Hirschhorn syndrome attributable to a 50% reduction in LETM1 expression level.
Haploinsufficiency of WHSC1 (Montrer WHSC1 Anticorps) and/or LETM1 contributes to Wolf-Hirschhorn Syndrome, but that loss of distinct and/or additional genes in 4p16.3 is necessary for the expression of the core Wolf-Hirschhorn Syndrome phenotype.
NCLX (Montrer SLC24A6 Anticorps), but not LETM1, mediates Ca(2 (Montrer CA2 Anticorps)+) extrusion from mitochondria. By controlling the duration of matrix Ca(2 (Montrer CA2 Anticorps)+) elevations, NCLX (Montrer SLC24A6 Anticorps) contributes to the regulation of NAD(P)H (Montrer NQO1 Anticorps) production and to the conversion of Ca(2 (Montrer CA2 Anticorps)+) signals into redox changes.
Functional properties of Letm1 described in study are remarkably similar to those of the H(+)-dependent Ca(2 (Montrer CA2 Anticorps)+) transport mechanism identified in intact mitochondria.
Data indicate that cellular Letm1 knockdown reduced Ca(2 (Montrer CA2 Anticorps)+)mito uptake, H(+)mito extrusion and impaired mitochondrial ATP generation capacity.
This gene encodes a protein that is localized to the inner mitochondrial membrane. The protein functions to maintain the mitochondrial tubular shapes and is required for normal mitochondrial morphology and cellular viability. Mutations in this gene cause Wolf-Hirschhorn syndrome, a complex malformation syndrome caused by the deletion of parts of the distal short arm of chromosome 4. Related pseudogenes have been identified on chromosomes 8, 15 and 19.
leucine zipper-EF-hand containing transmembrane protein 1
, LETM1 and EF-hand domain-containing protein 1, mitochondrial
, leucine zipper-EF-hand-containing transmembrane protein 1
, Leucine zipper-EF-hand-containing transmembrane protein 1
, LETM1 and EF-hand domain-containing protein 1, mitochondrial-like
, Mdm38 homolog