ATAD3B
 | This article may be too technical for most readers to understand. (May 2020) |
| ATAD3B | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | ATAD3B, AAA-TOB3, TOB3, ATPase family, AAA domain containing 3B, ATPase family AAA domain containing 3B | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 612317; GeneCards: ATAD3B | |||||||||||||||||||||||||||||||||||||||||||||||||||||
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| ATAD3B | |
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| Alliases | TOB3, AAA-TOB3, KIAA 1273 |
| External IDs | NCBI: AAH02542.1 |
| Gene Location (Human) | |
ATPase family AAA domain-containing protein 3B (or ATAD3B) is a protein that in humans is encoded by the ATAD3B gene.[3] ATAD3 is part of the AAA protein family.[3] The function of ATAD3B is not yet well understood by the scientific community.
Function
ATAD3B is associated with the mitochondria. The C terminus is anchored in the mitochondrial inter membrane space.[4]
The protein is linked with the pluripotency of stem cells. The ATAD3A gene is targeted by c-Myc[4] which is one of four factors needed to create induced pluripotent stem (i-PS) cells from mouse embryonic fibroblasts(MEFs).[5]
Its expression is linked to cell cycle function and tumor growth.[6] When ATAD3B was overexpressed, cell duplication took an extra three hours by spending a longer time in G1 phase.[6]
Dominant negative activity
A mutation in the stop codon means that ATAD3B protein 62 amino acids longer at the C-terminus compared to ATAD3A.[7] This C-terminal extension of ATAD3B turns it into a negative regulator of ATAD3A.[4]
Clinical significance
Abnormal expression levels of ATAD3B has been linked to chemoresistance. Overexpression of ATAD3B was the found to be the strongest factor in breast cancer survival rates.[8]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000160072 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ a b "Q5T9A4 · ATD3B_HUMAN". uniprot.org. UniProt consortium.
- ^ a b c Merle N, Féraud O, Gilquin B, Hubstenberger A, Kieffer-Jacquinot S, Assard N, et al. (July 2012). "ATAD3B is a human embryonic stem cell specific mitochondrial protein, re-expressed in cancer cells, that functions as dominant negative for the ubiquitous ATAD3A". Mitochondrion. 12 (4): 441–448. doi:10.1016/j.mito.2012.05.005. PMID 22664726.
- ^ Takahashi K, Yamanaka S (August 2006). "Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors". Cell. 126 (4): 663–676. doi:10.1016/j.cell.2006.07.024. hdl:2433/159777. PMID 16904174. S2CID 1565219.
- ^ a b Hubstenberger A, Labourdette G, Baudier J, Rousseau D (September 2008). "ATAD 3A and ATAD 3B are distal 1p-located genes differentially expressed in human glioma cell lines and present in vitro anti-oncogenic and chemoresistant properties". Experimental Cell Research. 314 (15): 2870–2883. doi:10.1016/j.yexcr.2008.06.017. PMID 18639545.
- ^ Li S, Rousseau D (February 2012). "ATAD3, a vital membrane bound mitochondrial ATPase involved in tumor progression". Journal of Bioenergetics and Biomembranes. 44 (1): 189–197. doi:10.1007/s10863-012-9424-5. PMID 22318359. S2CID 11106754.
- ^ Ovaska K, Matarese F, Grote K, Charapitsa I, Cervera A, Liu C, et al. (2013). Tucker-Kellogg G (ed.). "Integrative analysis of deep sequencing data identifies estrogen receptor early response genes and links ATAD3B to poor survival in breast cancer". PLOS Computational Biology. 9 (6) e1003100. Bibcode:2013PLSCB...9E3100O. doi:10.1371/journal.pcbi.1003100. PMC 3688481. PMID 23818839.
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