TIMM29

Last update 08 May 2025

Basic Info

Synonyms

C19orf52, Mitochondrial import inner membrane translocase subunit Tim29, TIM29

+ [2]

Introduction

Component of the TIM22 complex, a complex that mediates the import and insertion of multi-pass transmembrane proteins into the mitochondrial inner membrane. The TIM22 complex forms a twin-pore translocase that uses the membrane potential as the external driving force. Required for the stability of the TIM22 complex and functions in the assembly of the TIMM22 protein into the TIM22 complex. May facilitate cooperation between TIM22 and TOM complexes by interacting with TOMM40.

100 Clinical Results associated with TIMM29

100 Translational Medicine associated with TIMM29

0 Patents (Medical) associated with TIMM29

Literatures (Medical) associated with TIMM29

01 Apr 2025·Microbiology and Immunology

Analysis of the Functional Role of TIMM29 in the Hepatitis B Virus Life Cycle

Article

Author: Kimura‐Ohba, Shihoko ; Muriungi, Nelly ; Suwanmanee, Yadarat ; Ueda, Keiji ; Abueldahab, Limia ; Wada, Masami ; Ohsaki, Eriko

ABSTRACTHepatitis B virus (HBV) causes chronic hepatitis B, which can progress to liver cirrhosis and hepatocellular carcinoma. HBV has complex interactions with various cell organelles and proteins that ensure effective progeny virus production. We previously reported that a mitochondrial protein, TIMM29, should regulate the HBV life cycle through interactions with the HBV preS1 protein. Here, we established Halo‐TIMM29wt‐, Halo‐TIMM29:∆99–192‐, and Halo‐TIMM29:92–194‐expressing cells using TIMM29‐knockout HB611 (TIMM29KO/HB611) cells, a stably HBV‐producing cell line based on Huh6 cells. We found that HBV antigen expression and replication were downregulated in cells stably expressing full‐length TIMM29, but not in those expressing TIMM29 deletion mutants. On the other hand, in the case of TIMM29‐knockout C4 (TIMM29KO/C4), which is a human NTCP‐expressing HepG2 cell line that is competent for HBV infection and amplification, these phenomena were not reproduced, except in full‐length TIMM29 (Halo‐TIMM29wt)‐expressing cells. Using gene expression microarrays, we identified downregulation of ARRDC3 and BASP1 in TIMM29KO/HB611 and TIMM29KO/C4. It was suggested that TIMM29 localized at the mitochondrial inner membrane served as a signaling hub, orchestrating the activation of ARRDC3 and BASP1 expression to restrict HBV transcription. The expression of TIMM29 mutants in TIMM29KO/HB611 and TIMM29KO/C4 cells suggested that ARRDC3 was dependent on the HBV preS1‐binding region of TIMM29 (amino acids 99–189). In contrast, BASP1 expression varied according to cell type, indicating additional regulatory mechanisms. Thus, this study should significantly advance our understanding of TIMM29‐mediated inhibition of HBV amplification and lead to improvements in antiviral strategies and therapeutic interventions against HBV.

01 Feb 2024·Journal of Medical Virology

TIM22 and TIM29 inhibit HBV replication by up‐regulating SRSF1 expression

Article

Author: Long, Shao‐yuan ; Hu, Jie‐li ; Li, Jie ; Wei, Xia‐fei ; Huang, Ai‐long ; Lei, Ling ; Li, Shan ; Wang, Pei‐yun ; Wang, Jin‐lan ; Liu, Jia‐jun ; Guo, Lin

AbstractHepatitis B virus (HBV) infection is a serious global health problem. After the viruses infect the human body, the host can respond to the virus infection by coordinating various cellular responses, in which mitochondria play an important role. Evidence has shown that mitochondrial proteins are involved in host antiviral responses. In this study, we found that the overexpression of TIM22 and TIM29, the members of the inner membrane translocase TIM22 complex, significantly reduced the level of intracellular HBV DNA and RNA and secreted HBV surface antigens and E antigen. The effects of TIM22 and TIM29 on HBV replication and transcription is attributed to the reduction of core promoter activity mediated by the increased expression of SRSF1 which acts as a suppressor of HBV replication. This study provides new evidence for the critical role of mitochondria in the resistance of HBV infection and new targets for the development of treatment against HBV infection.

01 Dec 2020·Microbiology and ImmunologyQ4 · MEDICINE

TIMM29 interacts with hepatitis B virus preS1 to modulate the HBV life cycle

Q4 · MEDICINE

Article

Author: Muriungi, Nelly Gakii ; Ueda, Keiji

AbstractHepatitis B virus (HBV), a major global health problem, can cause chronic hepatitis, liver cirrhosis, and hepatocellular carcinomas in chronically infected patients. However, before HBV infection can be adequately controlled, many mysteries about the HBV life cycle must be solved. In this study, TIMM29, an inner mitochondrial membrane protein, was identified as an interaction partner of the preS1 region of the HBV large S protein. The interaction was verified by both an immunoprecipitation with preS1 peptides and a GST‐pulldown assay. Immunofluorescence studies also showed colocalization of preS1 and TIMM29. Moreover, it was determined that the preS1 bound with amino acids 92–189 of the TIMM29 protein. Infection of HBV in TIMM29‐overexpressing NTCP/G2 cells resulted in a significant decrease of HBeAg and both extracellular particle‐associated and core particle‐associated HBV DNA without affecting cccDNA formation. Comparable results were obtained with TIMM29‐overexpressing HB611 cells, which constitutively produce HBV. In contrast, knockout of TIMM29 in NTCP/G2 cells led to a higher production of HBV including HBeAg expression, as did knockout of TIMM29 in HB611. Collectively, these results suggested that TIMM29 interacts with the preS1 region of the HBV large S protein and modulates HBV amplification.

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TIMM29

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