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Review Open Access

LETM1 is required for mitochondrial homeostasis and cellular viability (Review)

  • Authors:
    • Yuwen Li
    • Quangdon Tran
    • Robin Shrestha
    • Longzhen Piao
    • Sungjin Park
    • Jisoo Park
    • Jongsun Park
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacology, Metabolic Syndrome and Cell Signaling Laboratory, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea, Department of Oncology, Affiliated Hospital of Yanbian University, Yanji, Jilin 133000, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3367-3375
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    Published online on: March 15, 2019
       https://doi.org/10.3892/mmr.2019.10041
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Abstract

Leucine zipper/EF‑hand‑containing transmembrane protein 1 (LETM1) has been identified as the gene responsible for Wolf‑Hirschhorn syndrome (WHS), which is characterized by intellectual disability, epilepsy, growth delay and craniofacial dysgenesis. LETM1 is a mitochondrial inner membrane protein that encodes a homolog of the yeast protein Mdm38, which is involved in mitochondrial morphology. In the present review, the importance of LETM1 in WHS and its role within the mitochondrion was explored. LETM1 governs the mitochondrion ion channel and is involved in mitochondrial respiration. Recent studies have reported that LETM1 acts as a mitochondrial Ca2+/H+ antiporter. LETM1 has also been identified as a K+/H+ exchanger, and serves a role in Mg2+ homeostasis. The function of LETM1 in mitochondria regulation is regulated by its binding partners, carboxyl‑terminal modulator protein and mitochondrial ribosomal protein L36. Therefore, we describe the remarkable role of LETM1 in mitochondrial network physiology and its function in mitochondrion‑mediated cell death. In the context of these findings, we suggest that the participation of LETM1 in tumorigenesis through the alteration of cancer metabolism should be investigated. This review provides a comprehensive description of LETM1 function, which is required for mitochondrial homeostasis and cellular viability.
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Copy and paste a formatted citation
Spandidos Publications style
Li Y, Tran Q, Shrestha R, Piao L, Park S, Park J and Park J: LETM1 is required for mitochondrial homeostasis and cellular viability (Review). Mol Med Rep 19: 3367-3375, 2019.
APA
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., & Park, J. (2019). LETM1 is required for mitochondrial homeostasis and cellular viability (Review). Molecular Medicine Reports, 19, 3367-3375. https://doi.org/10.3892/mmr.2019.10041
MLA
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., Park, J."LETM1 is required for mitochondrial homeostasis and cellular viability (Review)". Molecular Medicine Reports 19.5 (2019): 3367-3375.
Chicago
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., Park, J."LETM1 is required for mitochondrial homeostasis and cellular viability (Review)". Molecular Medicine Reports 19, no. 5 (2019): 3367-3375. https://doi.org/10.3892/mmr.2019.10041
Copy and paste a formatted citation
x
Spandidos Publications style
Li Y, Tran Q, Shrestha R, Piao L, Park S, Park J and Park J: LETM1 is required for mitochondrial homeostasis and cellular viability (Review). Mol Med Rep 19: 3367-3375, 2019.
APA
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., & Park, J. (2019). LETM1 is required for mitochondrial homeostasis and cellular viability (Review). Molecular Medicine Reports, 19, 3367-3375. https://doi.org/10.3892/mmr.2019.10041
MLA
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., Park, J."LETM1 is required for mitochondrial homeostasis and cellular viability (Review)". Molecular Medicine Reports 19.5 (2019): 3367-3375.
Chicago
Li, Y., Tran, Q., Shrestha, R., Piao, L., Park, S., Park, J., Park, J."LETM1 is required for mitochondrial homeostasis and cellular viability (Review)". Molecular Medicine Reports 19, no. 5 (2019): 3367-3375. https://doi.org/10.3892/mmr.2019.10041
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