anti-Leucine Zipper-EF-Hand Containing Transmembrane Protein 1 (LETM1) Antikörper

Human Leucine Zipper-EF-Hand Containing Transmembrane Protein 1 (LETM1) Interaktionspartner

1. 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.

2. 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]

3. these results revealed that the knockdown of LETM1 exhibited tumor suppressive effects, possibly by controlling the downstream Wnt/beta-catenin signaling pathway.

4. Data indicate a positive association between LETM1 up-regulation, YAP1 nuclear localization and high PDGFB expression.

5. LETM1 plays an important role in the progression of breast cancer

6. 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.

7. LETM1 plays an important role in the progression of head and neck squamous cell carcinoma.

8. 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.

9. Reconstitution of LETM1 or antioxidant overexpression rescued mitochondrial Ca(2+) transport and bioenergetics

10. These findings identify novel cellular phenotypes in Wolf-Hirschhorn syndrome attributable to a 50% reduction in LETM1 expression level.

11. 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.

12. 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.

13. Functional properties of Letm1 described in study are remarkably similar to those of the H(+)-dependent Ca(2+) transport mechanism identified in intact mitochondria.

14. 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.

15. 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.

16. Letm1 and UCP2/3 independently contribute to two distinct, mitochondrial Ca(2+) uptake pathways in intact endothelial cells.

17. we have identified a novel submicroscopic duplication involving dosage sensitive genes TACC3, FGFR3, and LETM1.

18. LETM1 suppressed lung cancer cell growth in vitro and in vivo.

19. LETM1 is evolutionarily conserved throughout the eukaryotic kingdom and located in the mitochondria.

20. Here, we present cellular and biochemical analysis of Letm1

Mouse (Murine) Leucine Zipper-EF-Hand Containing Transmembrane Protein 1 (LETM1) Interaktionspartner

1. This paper's findings delineate a mechanism by which PINK1 regulates mitochondrial Ca(2+) level through LETM1 and suggest a model by which PINK1 loss leads to deficient phosphorylation of LETM1 and impaired mitochondrial Ca(2+) transport.

2. Reconstitution of LETM1 or antioxidant overexpression rescued mitochondrial Ca(2+) transport and bioenergetics

3. Data indicate that cellular Letm1 knockdown reduced Ca(2+)mito uptake, H(+)mito extrusion and impaired mitochondrial ATP generation capacity.