関: ANT2

WordNet

(biochemistry) purine base found in DNA and RNA; pairs with thymine in DNA and with uracil in RNA (同)A
a phosphoric ester of a nucleoside; the basic structural unit of nucleic acids (DNA or RNA) (同)base

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アデニン(肝臓・茶の葉から採れる塩基の一種)

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1. 母体血中の無細胞核酸を使った非侵襲的出生前検査 noninvasive prenatal testing using cell free nucleic acids in maternal blood
2. 遺伝性疾患の基本原則 basic principles of genetic disease
3. 性感染症：思春期特有の問題の概要 sexually transmitted diseases overview of issues specific to adolescents
4. 性器潰瘍患者へのアプローチ approach to the patient with genital ulcers
5. 分子遺伝学の原理 principles of molecular genetics

English Journal

SIRT4 regulates ATP homeostasis and mediates a retrograde signaling via AMPK.

Ho L, Titus AS, Banerjee KK, George S, Lin W, Deota S, Saha AK, Nakamura K, Gut P, Verdin E, Kolthur-Seetharam U.Author information The Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA. Tata Institute of Fundamental Research, Homi Bhabha Road, Colaba, Mumbai, India.AbstractEfficient coupling of cellular energy production to metabolic demand is crucial to maintain organismal homeostasis. Here, we report that the mitochondrial Sirtuin Sirt4 regulates mitochondrial ATP homeostasis. We find that Sirt4 affects mitochondrial uncoupling via the adenine nucleotide translocator 2 (ANT2). Loss of Sirt4 expression leads to decreased cellular ATP levelsin vitro and in vivo while Sirt4 overexpression is associated with increased ATP levels. Further, we provide evidence that lack of Sirt4 activates a retrograde signaling response from the mitochondria to the nucleus that includes AMPK, PGC1α, key regulators of β-oxidation such as Acetyl-CoA carboxylase, and components of the mitochondrial respiratory machinery. This study highlights the ability of Sirt4 to regulate ATP levels via ANT2 and a feedback loop involving AMPK.
Aging.Aging (Albany NY).2013 Nov 26. [Epub ahead of print]
Efficient coupling of cellular energy production to metabolic demand is crucial to maintain organismal homeostasis. Here, we report that the mitochondrial Sirtuin Sirt4 regulates mitochondrial ATP homeostasis. We find that Sirt4 affects mitochondrial uncoupling via the adenine nucleotide translocato
PMID 24296486

The mitochondrial solute carrier SLC25A5 at Xq24 is a novel candidate gene for non-syndromic intellectual disability.

Vandewalle J, Bauters M, Van Esch H, Belet S, Verbeeck J, Fieremans N, Holvoet M, Vento J, Spreiz A, Kotzot D, Haberlandt E, Rosenfeld J, Andrieux J, Delobel B, Dehouck MB, Devriendt K, Fryns JP, Marynen P, Goldstein A, Froyen G.Author information Human Genome Laboratory, VIB Center for the Biology of Disease, Leuven, Belgium.AbstractLoss-of-function mutations in several different neuronal pathways have been related to intellectual disability (ID). Such mutations often are found on the X chromosome in males since they result in functional null alleles. So far, microdeletions at Xq24 reported in males always have been associated with a syndromic form of ID due to the loss of UBE2A. Here, we report on overlapping microdeletions at Xq24 that do not include UBE2A or affect its expression, in patients with non-syndromic ID plus some additional features from three unrelated families. The smallest region of overlap, confirmed by junction sequencing, harbors two members of the mitochondrial solute carrier family 25, SLC25A5 and SLC25A43. However, identification of an intragenic microdeletion including SLC25A43 but not SLC25A5 in a healthy boy excluded a role for SLC25A43 in cognition. Therefore, our findings point to SLC25A5 as a novel gene for non-syndromic ID. This highly conserved gene is expressed ubiquitously with high levels in cortex and hippocampus, and a presumed role in mitochondrial exchange of ADP/ATP. Our data indicate that SLC25A5 is involved in memory formation or establishment, which could add mitochondrial processes to the wide array of pathways that regulate normal cognitive functions.
Human genetics.Hum Genet.2013 Oct;132(10):1177-85. doi: 10.1007/s00439-013-1322-3. Epub 2013 Jun 20.
Loss-of-function mutations in several different neuronal pathways have been related to intellectual disability (ID). Such mutations often are found on the X chromosome in males since they result in functional null alleles. So far, microdeletions at Xq24 reported in males always have been associated
PMID 23783460

Many faces of mitochondrial uncoupling during age: damage or defense?

Bellanti F, Romano AD, Giudetti AM, Rollo T, Blonda M, Tamborra R, Vendemiale G, Serviddio G.Author information Dipartimento di Scienze Mediche e Chirurgiche, Università di Foggia 71122, Foggia, Italy. g.vendemiale@unifg.itAbstractAn increased mitochondrial proton leak occurs in aging, but the origin of such modification remains unclear. This study defined the cause of mitochondrial uncoupling in mitotic (liver) and postmitotic (heart) rat tissues during aging and its effects on energy homeostasis and free radical production. Proton leak in old heart mitochondria was dependent on uncoupling proteins' upregulation, whereas it was caused by alterations in the mitochondrial membrane composition in old liver. ATP homeostasis was impaired in both tissues from old animals and was associated to disrupted F0F1-ATPase activity. H2O2 production rate and 4-hydroxy-2-nonenalprotein adducts were higher in old liver mitochondria compared with young liver mitochondria, but they were similar in heart mitochondria from both groups. Moreover, key mitochondrial biogenesis regulators were upregulated in old liver but downregulated in old heart. In conclusion, uncoupling proteins mediate proton leak and avoid oxidative damage in heart, acting as a protective mechanism. This does not occur in liver, where ATP depletion and oxidative stress may stimulate mitochondrial biogenesis and eliminate damaged cells.
The journals of gerontology. Series A, Biological sciences and medical sciences.J Gerontol A Biol Sci Med Sci.2013 Aug;68(8):892-902. doi: 10.1093/gerona/gls332. Epub 2013 Jan 4.
An increased mitochondrial proton leak occurs in aging, but the origin of such modification remains unclear. This study defined the cause of mitochondrial uncoupling in mitotic (liver) and postmitotic (heart) rat tissues during aging and its effects on energy homeostasis and free radical production.
PMID 23292290

Japanese Journal

Genetic analysis of two Japanese families with progressive external ophthalmoplegia and parkinsonism.

Sato Kazunori,Yabe Ichiro,Yaguchi Hiroaki,Nakano Fumihito,Kunieda Yasuyuki,Saitoh Shinji,Sasaki Hidenao
Journal of neurology 258(7), 1327-1332, 2011-07
… Mutations in the progressive external ophthalmoplegia 1 (PEO1), adenine nucleotide translocator 1 (ANT1) and DNA polymerase gamma (POLG) genes were reported in patients with progressive external ophthalmoplegia and parkinsonism. …
NAID 120004405523

Drug Development Targeting the Glycogen Synthase Kinase-3β (GSK-3β)-Mediated Signal Transduction Pathway : Role of GSK-3β in Myocardial Protection Against Ischemia/Reperfusion Injury

Miura Tetsuji,Nishihara Masahiro,Miki Takayuki
Journal of pharmacological sciences 109(2), 162-167, 2009-02-20
… The mPTP primarily consists of adenine nucleotide translocator (ANT) and voltage-dependent anion channel, and its opening is triggered by binding of cyclophilin-D (CyP-D) to ANT, which increases Ca2+ sensitivity of the mPTP. …
NAID 10025734088

PE-072 Ischemic Preconditioning Prevents Ischemia/reperfusion-Induced Dephosphorylation of Mitochondrial Connexin-43 in a Protein Complex with Adenine Nucleotide Translocator(Myocardial ischemia/reperfusion, basic/clinical-2, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Takahashi Akari,Miura Tetsuji,Miki Takayuki,Yano Toshiyuki,Naitoh Kazuyuki,Nishihara Masahiro,Satoh Takahiro,Shimamoto Kazuaki
Circulation journal : official journal of the Japanese Circulation Society 71(Supplement_I), 342-343, 2007-03-01
NAID 110006397175

★リンクテーブル★

リンク元	「ANT2」「アデニンヌクレオチドトランスロケーター2」「SLC25A5」
関連記事	「translocator」「adenine nucleotide」