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Here, the authors show that LETM1 is associated with mitochondrial ribosomes, is required for mitochondrial DNA distribution and expression, and regulates the activity of an ancillary metabolic enzyme, pyruvate dehydrogenase.
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Data show that LETM1 is a transporter protein localized to the inner mitochondrial membrane shown to have a Ca(2+)/H exchanger activity. The role of LETM1 to Ca(2+) regulation is evident from Wolf-Hirschhorn syndrome patients that harbor a haploinsuficiency in LETM1 expression, leading to dysfunctional mitochondrial Ca(2+) handling and from many types of cancer cells that show an upregulation of its expression. [review]
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these results revealed that the knockdown of LETM1 exhibited tumor suppressive effects, possibly by controlling the downstream Wnt/beta-catenin signaling pathway.
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Data indicate a positive association between LETM1 up-regulation, YAP1 nuclear localization and high PDGFB expression.
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LETM1 plays an important role in the progression of breast cancer
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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.
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LETM1 plays an important role in the progression of head and neck squamous cell carcinoma.
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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 expression, which is associated with susceptibility to seizures.
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Reconstitution of LETM1 or antioxidant overexpression rescued mitochondrial Ca(2+) transport and bioenergetics
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These findings identify novel cellular phenotypes in Wolf-Hirschhorn syndrome attributable to a 50% reduction in LETM1 expression level.
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Haploinsufficiency of WHSC1 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.
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NCLX, but not LETM1, mediates Ca(2+) extrusion from mitochondria. By controlling the duration of matrix Ca(2+) elevations, NCLX contributes to the regulation of NAD(P)H production and to the conversion of Ca(2+) signals into redox changes.
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Functional properties of Letm1 described in study are remarkably similar to those of the H(+)-dependent Ca(2+) transport mechanism identified in intact mitochondria.
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Data indicate that loss of Letm1 contributes to the pathology of Wolf-Hirschhorn syndrome and may contribute to seizure phenotypes by reducing glucose oxidation and other specific metabolic alterations.
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Summarizes the current state of the art about the functions of LETM1 and its role in pathophysiology, with some emphasis on whether it is a feasible candidate for regulation of mitochondrial Ca2+ homeostasis.
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Letm1 and UCP2/3 independently contribute to two distinct, mitochondrial Ca(2+) uptake pathways in intact endothelial cells.
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we have identified a novel submicroscopic duplication involving dosage sensitive genes TACC3, FGFR3, and LETM1.
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LETM1 suppressed lung cancer cell growth in vitro and in vivo.
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LETM1 is evolutionarily conserved throughout the eukaryotic kingdom and located in the mitochondria.
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Here, we present cellular and biochemical analysis of Letm1
