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LETM1 encodes a protein that is localized to the inner mitochondrial membrane. Additionally we are shipping LETM1 Proteins (5) and many more products for this protein.
Showing 10 out of 78 products:
Human Monoclonal LETM1 Primary Antibody for 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. in Human molecular genetics 2008
Show all 6 Pubmed References
Human Polyclonal LETM1 Primary Antibody for 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. in Journal of cell science 2012
Human Polyclonal LETM1 Primary Antibody for 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. in Nature cell biology 2012
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 (show MT-CYB Antibodies) expression, which is associated with susceptibility to seizures.
Reconstitution of LETM1 or antioxidant overexpression rescued mitochondrial Ca(2 (show CA2 Antibodies)+) 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 (show WHSC1 Antibodies) 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 (show SLC24A6 Antibodies), but not LETM1, mediates Ca(2 (show CA2 Antibodies)+) extrusion from mitochondria. By controlling the duration of matrix Ca(2 (show CA2 Antibodies)+) elevations, NCLX (show SLC24A6 Antibodies) contributes to the regulation of NAD(P)H (show NQO1 Antibodies) production and to the conversion of Ca(2 (show CA2 Antibodies)+) signals into redox changes.
Functional properties of Letm1 described in study are remarkably similar to those of the H(+)-dependent Ca(2 (show CA2 Antibodies)+) transport mechanism identified in intact mitochondria.
Data indicate that loss of Letm1 contributes to the path (show CA2 Antibodies)ology of Wolf-Hirschhorn syndrome and may contribute to seizure phenotypes by reducing glucose oxidation and other specific metabolic alterations.
Data indicate that cellular Letm1 knockdown reduced Ca(2 (show CA2 Antibodies)+)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