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Gene Symbol |
ATP5F1B |
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Aliases |
ATP5B, ATPMB, ATPSB, HEL-S-271 |
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Entrez Gene ID |
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Gene Name |
ATP synthase F1 subunit beta |
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Chromosomal Location |
12q13.3 |
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HGNC ID |
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Summary |
This gene encodes a subunit of mitochondrial ATP synthase. Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. ATP synthase is composed of two linked multi-subunit complexes: the soluble catalytic core, F1, and the membrane-spanning component, Fo, comprising the proton channel. The catalytic portion of mitochondrial ATP synthase consists of 5 different subunits (alpha, beta, gamma, delta, and epsilon) assembled with a stoichiometry of 3 alpha, 3 beta, and a single representative of the other 3. The proton channel consists of three main subunits (a, b, c). This gene encodes the beta subunit of the catalytic core. [provided by RefSeq, Jul 2008]
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e!Ensembl
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Gene Ontology (GO)
| GO ID |
Ontology |
Function |
Evidence |
Reference |
| GO:0001525 |
Biological process |
Angiogenesis |
IMP |
17510399 |
| GO:0001649 |
Biological process |
Osteoblast differentiation |
HDA |
16210410 |
| GO:0006091 |
Biological process |
Generation of precursor metabolites and energy |
NAS |
2870059 |
| GO:0006754 |
Biological process |
ATP biosynthetic process |
IMP |
17510399, 21106936 |
| GO:0042776 |
Biological process |
Mitochondrial ATP synthesis coupled proton transport |
IBA |
21873635 |
| GO:0042776 |
Biological process |
Mitochondrial ATP synthesis coupled proton transport |
IC |
12110673 |
| GO:0043536 |
Biological process |
Positive regulation of blood vessel endothelial cell migration |
IGI |
21106936 |
| GO:0051453 |
Biological process |
Regulation of intracellular pH |
IMP |
17510399 |
| GO:1902600 |
Biological process |
Proton transmembrane transport |
IMP |
17510399 |
| GO:0005634 |
Cellular component |
Nucleus |
HDA |
21630459 |
| GO:0005739 |
Cellular component |
Mitochondrion |
HDA |
20833797 |
| GO:0005739 |
Cellular component |
Mitochondrion |
IDA |
2870059 |
| GO:0005753 |
Cellular component |
Mitochondrial proton-transporting ATP synthase complex |
IBA |
21873635 |
| GO:0005753 |
Cellular component |
Mitochondrial proton-transporting ATP synthase complex |
IDA |
12110673 |
| GO:0005754 |
Cellular component |
Mitochondrial proton-transporting ATP synthase, catalytic core |
NAS |
2870059 |
| GO:0005759 |
Cellular component |
Mitochondrial matrix |
NAS |
2687158 |
| GO:0005886 |
Cellular component |
Plasma membrane |
IDA |
10077593 |
| GO:0009986 |
Cellular component |
Cell surface |
IDA |
17510399 |
| GO:0016020 |
Cellular component |
Membrane |
HDA |
16210410, 19946888 |
| GO:0016020 |
Cellular component |
Membrane |
IDA |
21106936 |
| GO:0031966 |
Cellular component |
Mitochondrial membrane |
IDA |
8006588 |
| GO:0042645 |
Cellular component |
Mitochondrial nucleoid |
IDA |
18063578 |
| GO:0045259 |
Cellular component |
Proton-transporting ATP synthase complex |
IDA |
21106936 |
| GO:0045261 |
Cellular component |
Proton-transporting ATP synthase complex, catalytic core F(1) |
IBA |
21873635 |
| GO:0070062 |
Cellular component |
Extracellular exosome |
HDA |
19056867, 19199708, 20458337, 23533145 |
| GO:0005515 |
Molecular function |
Protein binding |
IPI |
10077593, 11410595, 15161933, 20618440, 21106936 |
| GO:0016887 |
Molecular function |
ATPase activity |
IBA |
21873635 |
| GO:0016887 |
Molecular function |
ATPase activity |
IDA |
12110673 |
| GO:0022857 |
Molecular function |
Transmembrane transporter activity |
IC |
12110673 |
| GO:0042288 |
Molecular function |
MHC class I protein binding |
IDA |
17643490 |
| GO:0043532 |
Molecular function |
Angiostatin binding |
IPI |
21106936 |
| GO:0046933 |
Molecular function |
Proton-transporting ATP synthase activity, rotational mechanism |
IBA |
21873635 |
| GO:0046933 |
Molecular function |
Proton-transporting ATP synthase activity, rotational mechanism |
IMP |
21106936 |
| GO:0046961 |
Molecular function |
Proton-transporting ATPase activity, rotational mechanism |
IMP |
17510399 |
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| Protein Information |
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Protein Name |
ATP synthase subunit beta, mitochondrial, ATP synthase, H+ transporting, mitochondrial F1 complex, beta polypeptide, epididymis secretory protein Li 271, mitochondrial ATP synthase beta subunit, mitochondrial ATP synthetase, beta subunit |
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Function |
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Mitochondrial membrane ATP synthase (F(1)F(0) ATP synthase or Complex V) produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain. F-type ATPases consist of two structural domains, F(1) - containing the extramembraneous catalytic core, and F(0) - containing the membrane proton channel, linked together by a central stalk and a peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F(1) is coupled via a rotary mechanism of the central stalk subunits to proton translocation. Subunits alpha and beta form the catalytic core in F(1). Rotation of the central stalk against the surrounding alpha(3)beta(3) subunits leads to hydrolysis of ATP in three separate catalytic sites on the beta subunits |
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UniProt |
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Interactions |
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| STRING |
MINT |
IntAct |
| ENSP00000263867 |
P40121 |
P40121 |
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View interactions
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Associated Diseases
| Disease group | Disease Name | References |
| Endocrine System Diseases |
| PCOS |
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| Nervous System Diseases |
| Spinocerebellar ataxia |
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| Renal Disorder |
| Kidney Failure |
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| Kidney Insufficiency |
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References |
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| Li Wei, Li Sai-Jiao, Yin Tai-Lang, Yang Jing, Cheng Yan |
| Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.| Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.| Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.| Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, 430060, China. Dryangqing@hotmail.com.| Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, 430060, China. |
| J Huazhong Univ Sci Technolog Med Sci. 2017 Apr;37(2):210-216. doi: |
Abstract
This study investigated the abnormal expression of ATP synthase beta-subunit (ATPsyn-beta) in pancreas islets of rat model of polycystic ovary syndrome (PCOS) with type 2 diabetes mellitus (T2DM), and the secretion function changes after up-regulation of ATP5b. Sixty female SD rats were divided into three groups randomly and equally. The rat model of PCOS with T2DM was established by free access to the high-carbohydrate/high-fat diet, subcutaneous injections of DHEA, and a single injection of streptozotocin. The pancreas was removed for the detection of the ATPsyn-beta expression by immunohistochemical staining, Western blotting and reverse transcription-PCR (RT-PCR). The pancreas islets of the rats were cultured, isolated with collagenase V and purified by gradient centrifugation, and the insulin secretion after treatment with different glucose concentrations was tested. Lentivirus ATP5b was successfully constructed with the vector of GV208 and transfected into the pancreas islets for the over-expression of ATPsyn-beta. The insulin secretion and intracellular ATP content were determined after transfection of the PCOS-T2DM pancreas islets with Lenti-ATP5b. The results showed that the expression of ATPsyn-beta protein and mRNA was significantly decreased in the pancreas of PCOS-T2DM rats. The ATP content in the pancreas islets was greatly increased and the insulin secretion was improved after the up-regulation of ATPsyn-beta in the pancreas islets transfected with lenti-ATP5b. These results indicated that for PCOS, the ATPsyn-beta might be one of the key factors for the attack of T2DM. |
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