activating transcription factor 6

活性化転写因子6

関

ATF6

WordNet

1. be a contributing factor; "make things factor into a companys profitability"
2. any of the numbers (or symbols) that form a product when multiplied together
3. an independent variable in statistics
4. anything that contributes causally to a result; "a number of factors determined the outcome"
5. consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
6. resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
7. an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
8. a concept whose truth can be proved; "scientific hypotheses are not facts"
9. a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
10. a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
11. (genetics) the organic process whereby the DNA sequence in a gene is copied into mRNA; the process whereby a base sequence of messenger RNA is synthesized on a template of complementary DNA
12. a sound or television recording (e.g., from a broadcast to a tape recording)
13. something written, especially copied from one medium to another, as a typewritten version of dictation (同)written text
14. causing motion or action or change (同)actuating

PrepTutorEJDIC

1. (…の)『要因』,(…を生み出す)要素《+『in』+『名』(do『ing』)》 / 囲数,約数 / 代理人,《おもに英》仲買人 / =factorize
2. 〈C〉『事実』,実際にある(あった)事 / 〈U〉真相,真実(truth) / 《the~》(法律用語で)犯行
3. 〈U〉(…を)書き写す(書き直す)こと,(…の)転写,謄写《+of+名》 / 〈C〉写し(書き直し)[たもの] / 〈U〉〈C〉編曲[されたもの] / 〈U〉〈C〉(ラジオ・テレビの)録音(録画)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/06 17:49:06」(JST)

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[Wiki en表示]

Activating transcription factor 6
Identifiers
Symbols	ATF6; ATF6A
External IDs	OMIM: 605537 MGI: 1926157 HomoloGene: 32015 GeneCards: ATF6 Gene
Gene Ontology Molecular function • sequence-specific DNA binding transcription factor activity • transcription coactivator activity • protein binding • sequence-specific DNA binding Cellular component • Golgi membrane • nucleus • nuclear envelope • nucleoplasm • endoplasmic reticulum membrane • integral to membrane Biological process • transcription, DNA-dependent • regulation of transcription from RNA polymerase II promoter • protein folding • response to stress • activation of signaling protein activity involved in unfolded protein response • positive regulation of transcription from RNA polymerase II promoter involved in unfolded protein response • signal transduction • endoplasmic reticulum unfolded protein response Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	22926	226641
Ensembl	ENSG00000118217	ENSMUSG00000026663
UniProt	P18850	n/a
RefSeq (mRNA)	NM_007348	NM_001081304
RefSeq (protein)	NP_031374	NP_001074773
Location (UCSC)	Chr 1: 161.74 – 161.93 Mb	Chr 1: 170.7 – 170.87 Mb
PubMed search	[1]	[2]

Activating transcription factor 6, also known as ATF6, is a protein that, in humans, is encoded by the ATF6 gene and is involved in the unfolded protein response.

Function

ATF6 is an endoplasmic reticulum (ER) stress-regulated transmembrane transcription factor that activates the transcription of ER molecules. Accumulation of misfolded proteins in the Endoplasmic Reticulum results in the proteolytic cleavage of ATF6. The cytosolic portion of ATF6 will move to the nucleus and act as a transcription factor to cause the transcription of ER chaperones.

See also

• Activating transcription factor

Interactions

ATF6 has been shown to interact with YY1 and Serum response factor.

References

Further reading

• Hai T, Hartman MG (2001). "The molecular biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors: activating transcription factor proteins and homeostasis". Gene 273 (1): 1–11. doi:10.1016/S0378-1119(01)00551-0. PMID 11483355. 
• Hai TW, Liu F, Coukos WJ, Green MR (1990). "Transcription factor ATF cDNA clones: an extensive family of leucine zipper proteins able to selectively form DNA-binding heterodimers". Genes Dev. 3 (12B): 2083–90. doi:10.1101/gad.3.12b.2083. PMID 2516827. 
• Zhu C, Johansen FE, Prywes R (1997). "Interaction of ATF6 and serum response factor". Mol. Cell. Biol. 17 (9): 4957–66. PMC 232347. PMID 9271374. 
• Yoshida H, Haze K, Yanagi H, et al. (1999). "Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors". J. Biol. Chem. 273 (50): 33741–9. doi:10.1074/jbc.273.50.33741. PMID 9837962. 
• Haze K, Yoshida H, Yanagi H, et al. (1999). "Mammalian Transcription Factor ATF6 Is Synthesized as a Transmembrane Protein and Activated by Proteolysis in Response to Endoplasmic Reticulum Stress". Mol. Biol. Cell 10 (11): 3787–99. PMC 25679. PMID 10564271. 
• Li M, Baumeister P, Roy B, et al. (2000). "ATF6 as a Transcription Activator of the Endoplasmic Reticulum Stress Element: Thapsigargin Stress-Induced Changes and Synergistic Interactions with NF-Y and YY1". Mol. Cell. Biol. 20 (14): 5096–106. doi:10.1128/MCB.20.14.5096-5106.2000. PMC 85959. PMID 10866666. 
• Yoshida H, Okada T, Haze K, et al. (2001). "Endoplasmic Reticulum Stress-Induced Formation of Transcription Factor Complex ERSF Including NF-Y (CBF) and Activating Transcription Factors 6α and 6β That Activates the Mammalian Unfolded Protein Response". Mol. Cell. Biol. 21 (4): 1239–48. doi:10.1128/MCB.21.4.1239-1248.2001. PMC 99577. PMID 11158310. 
• Ye J, Rawson RB, Komuro R, et al. (2001). "ER stress induces cleavage of membrane-bound ATF6 by the same proteases that process SREBPs". Mol. Cell 6 (6): 1355–64. doi:10.1016/S1097-2765(00)00133-7. PMID 11163209. 
• Parker R, Phan T, Baumeister P, et al. (2001). "Identification of TFII-I as the Endoplasmic Reticulum Stress Response Element Binding Factor ERSF: Its Autoregulation by Stress and Interaction with ATF6". Mol. Cell. Biol. 21 (9): 3220–33. doi:10.1128/MCB.21.9.3220-3233.2001. PMC 86961. PMID 11287625. 
• Gotoh T, Oyadomari S, Mori K, Mori M (2002). "Nitric oxide-induced apoptosis in RAW 264.7 macrophages is mediated by endoplasmic reticulum stress pathway involving ATF6 and CHOP". J. Biol. Chem. 277 (14): 12343–50. doi:10.1074/jbc.M107988200. PMID 11805088. 
• Chen X, Shen J, Prywes R (2002). "The luminal domain of ATF6 senses endoplasmic reticulum (ER) stress and causes translocation of ATF6 from the ER to the Golgi". J. Biol. Chem. 277 (15): 13045–52. doi:10.1074/jbc.M110636200. PMID 11821395. 
• Thuerauf DJ, Morrison LE, Hoover H, Glembotski CC (2002). "Coordination of ATF6-mediated transcription and ATF6 degradation by a domain that is shared with the viral transcription factor, VP16". J. Biol. Chem. 277 (23): 20734–9. doi:10.1074/jbc.M201749200. PMID 11909875. 
• Okada T, Yoshida H, Akazawa R, et al. (2002). "Distinct roles of activating transcription factor 6 (ATF6) and double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase (PERK) in transcription during the mammalian unfolded protein response". Biochem. J. 366 (Pt 2): 585–94. doi:10.1042/BJ20020391. PMC 1222788. PMID 12014989. 
• Luo S, Lee AS (2002). "Requirement of the p38 mitogen-activated protein kinase signalling pathway for the induction of the 78 kDa glucose-regulated protein/immunoglobulin heavy-chain binding protein by azetidine stress: activating transcription factor 6 as a target for stress-induced phosphorylation". Biochem. J. 366 (Pt 3): 787–95. doi:10.1042/BJ20011802. PMC 1222838. PMID 12076252. 
• Tardif KD, Mori K, Siddiqui A (2002). "Hepatitis C Virus Subgenomic Replicons Induce Endoplasmic Reticulum Stress Activating an Intracellular Signaling Pathway". J. Virol. 76 (15): 7453–9. doi:10.1128/JVI.76.15.7453-7459.2002. PMC 136367. PMID 12097557. 
• Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932. 
• Shuda M, Kondoh N, Imazeki N, et al. (2004). "Activation of the ATF6, XBP1 and grp78 genes in human hepatocellular carcinoma: a possible involvement of the ER stress pathway in hepatocarcinogenesis". J. Hepatol. 38 (5): 605–14. doi:10.1016/S0168-8278(03)00029-1. PMID 12713871. 
• Okada T, Haze K, Nadanaka S, et al. (2003). "A serine protease inhibitor prevents endoplasmic reticulum stress-induced cleavage but not transport of the membrane-bound transcription factor ATF6". J. Biol. Chem. 278 (33): 31024–32. doi:10.1074/jbc.M300923200. PMID 12782636. 
• Newman JR, Keating AE (2003). "Comprehensive identification of human bZIP interactions with coiled-coil arrays". Science 300 (5628): 2097–101. doi:10.1126/science.1084648. PMID 12805554. 

External links

• ATF6 protein, human at the US National Library of Medicine Medical Subject Headings (MeSH)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

UpToDate Contents

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English Journal

• Acrolein activates cell survival and apoptotic death responses involving the endoplasmic reticulum in A549 lung cells.

• Tanel A1, Pallepati P1, Bettaieb A1, Morin P1, Averill-Bates DA2.Author information 1Département des Sciences Biologiques (TOXEN), Université du Québec à Montréal, CP 8888, Succursale Centre-ville, Montréal, Québec H3C 3P8, Canada.2Département des Sciences Biologiques (TOXEN), Université du Québec à Montréal, CP 8888, Succursale Centre-ville, Montréal, Québec H3C 3P8, Canada. Electronic address: averill.diana@uqam.ca.AbstractAcrolein, a highly reactive α,β-unsaturated aldehyde, is a product of endogenous lipid peroxidation. It is a ubiquitous environmental pollutant that is generated mainly by smoke, overheated cooking oil and vehicle exhaust. Acrolein damages cellular proteins, which could lead to accumulation of aberrantly-folded proteins in the endoplasmic reticulum (ER). This study determines the mechanisms involved in acrolein-induced apoptosis mediated by the ER and possible links with the ER stress response in human A549 lung cells. The exposure of cells to acrolein (15-50μM) for shorter times of 15 to 30min activated several ER stress markers. These included the ER chaperone protein BiP and the three ER sensors: (i) the survival/rescue molecules protein kinase RNA (PKR)-like ER kinase (PERK) and eukaryotic initiation factor 2 alpha (eIF2α) were phosphorylated; (ii) cleavage of activating transcription factor 6 (ATF6) occurred, and (iii) inositol-requiring protein-1 alpha (IRE1α) was phosphorylated. Acrolein (25-50μM) caused apoptotic cell death mediated by the ER after 2h, which was characterised by the induction of CHOP and activation of ER proteases calpain and caspase-4. Calpain and caspase-7 were the initiating factors for caspase-4 activation in acrolein-induced apoptosis. These results increase our knowledge about cellular responses to acrolein in lung cells, which have implications for human health.
• Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1843(5):827-35. doi: 10.1016/j.bbamcr.2013.12.012. Epub 2013 Dec 26.
• Acrolein, a highly reactive α,β-unsaturated aldehyde, is a product of endogenous lipid peroxidation. It is a ubiquitous environmental pollutant that is generated mainly by smoke, overheated cooking oil and vehicle exhaust. Acrolein damages cellular proteins, which could lead to accumulation of abe
• PMID 24373849

• Role of unfolded protein response in affecting osteoblast differentiation induced by fluoride.

• Li XN1, Lv P, Sun Z, Li GS, Xu H.Author information 1Department of Endemic Diseases, Jilin University, Changchun, 130021, People's Republic of China.AbstractThe objective of this study was to determine the expression of classic bone markers and unfolded protein response (UPR) signaling factors through MC3T3-E1 cells exposed to varying concentrations of fluoride. Excessive fluoride exposure caused the skeletal disease. During this process, osteoblasts played a critical role in the advanced skeletal fluorosis. Recent literature showed that endoplasmic reticulum (ER) stress and UPR were involved in numerous aspects of bone biology. Our results indicated that co-exposure of low-dose fluoride and mineral induction medium stimulated the expression of alkaline phosphatase, runt-related transcription factor 2 (Runx2), and osterix in MC3T3-E1 cells. Accordingly, the expression of double-stranded RNA-activated protein kinase (PKR)-like ER kinase, activating transcription factor 6, and X-box binding protein 1 also increased under the same fluoride exposure condition. The upregulation of three UPR factors was similar with osteogenic differentiation markers and transcription factors, which implied the relation between osteoblast differentiation and UPR pathways. Moreover, the role of UPR affecting osteoblast differentiation was investigated by decreasing the expression of binding immunoglobulin protein (BiP) mRNA through small interfering RNA (siRNA) technique. BiP knockdown led to suppress activation of UPR pathways. The deletion of BiP expression hardly stimulated the osteogenic cells differentiation but inhibited cell function under fluoride and mineralization induction exposure. In conclusion, fluoride had dual effect on osteogenic action. The UPR possibly involved in the mechanism of osteoblasts differentiation induced by fluoride.
• Biological trace element research.Biol Trace Elem Res.2014 Apr;158(1):113-21. doi: 10.1007/s12011-014-9897-7. Epub 2014 Feb 13.
• The objective of this study was to determine the expression of classic bone markers and unfolded protein response (UPR) signaling factors through MC3T3-E1 cells exposed to varying concentrations of fluoride. Excessive fluoride exposure caused the skeletal disease. During this process, osteoblasts pl
• PMID 24522478

• Functions and mechanisms of intermittent negative pressure for osteogenesis in human bone marrow mesenchymal stem cells.

• Yang Z, Yao JF, Xu P, Zhang JB, Zhang YM, Zhu YJ, Qin SQ, Liu L, Liu H, Hou WK, Xu K.Author information Department of Joint Surgery, Hong Hui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710054, P.R. China.AbstractThe present study aimed to determine the mechanism by which low‑intensity intermittent negative pressure affects the differentiation and proliferation of human mesenchymal stem cells (MSCs). Alkaline phosphatase (ALP) activity, type I collagen and vascular endothelial growth factor (VEGF) were detected to analyze differentiation. MTT and flow cytometry were employed to measure proliferation and apoptosis. Western blot analysis was used to examine endoplasmic reticulum (ER) stress‑associated factors. This study was divided into two groups, including a normal group (without any treatment) and vacuum group (treated with a vacuum). There was a significant decrease in the proliferation of cells in the vacuum group. The number of cells in S phase was reduced significantly, while the rate of apoptosis and the activity of ALP were markedly increased under vacuum conditions. Expression of collagen type I and VEGF was significantly increased, and the ratio of osteoprotegrin to osteoprotegrin ligand was decreased significantly in the vacuum group. ER stress‑associated proteins, p‑PRKR‑like ER kinase, inositol‑requiring enzyme 1 and cleaved activating transcription factor 6, as well as the downstream factors, were activated when treated with negative pressure. In conclusion, treatment with low‑intensity and intermittent negative pressure may inhibit the proliferation of MSCs and trigger ER stress‑associated cellular apoptosis, further enhancing osteogenesis activity and inducing differentiation to osteoblasts.
• Molecular medicine reports.Mol Med Rep.2014 Apr;9(4):1331-6. doi: 10.3892/mmr.2014.1968. Epub 2014 Feb 19.
• The present study aimed to determine the mechanism by which low‑intensity intermittent negative pressure affects the differentiation and proliferation of human mesenchymal stem cells (MSCs). Alkaline phosphatase (ALP) activity, type I collagen and vascular endothelial growth factor (VEGF) were det
• PMID 24567078

Japanese Journal

• Activating transcription factor 5 enhances radioresistance and malignancy in cancer cells

• Ishihara Seiichiro,Yasuda Motoaki,Ishizu Akihiro,Ishikawa Masayori,Shirato Hiroki,Haga Hisashi
• Oncotarget 6(7), 4602-4614, 2015-03-10
• … Here, we show that activating transcription factor 5 (ATF5) promotes radioresistance and malignancy in cancer cells after irradiation. …
• NAID 120005613573

• LIM-homeodomain transcription factor Awh is a key component activating all three fibroin genes, fibH, fibL and fhx, in the silk gland of the silkworm, Bombyx mori

• Kimoto Mai,Tsubota Takuya,Uchino Keiro,Sezutsu Hideki,Takiya Shigeharu
• Insect biochemistry and molecular biology 56, 29-35, 2015-01
• … Silk gland factor-2 (SGF-2) is a PSG-specific activator complex of fibH, composed of a LIM-homeodomain protein, Awh, and its cofactors, Ldb and Lcaf. …
• NAID 120005567736

• ATF3 Inhibits Tenascin-C-induced Foam Cell Formation in LPS-Stimulated THP-1 Macrophages by Suppressing TLR-4

• Luo Hong,Wang Jing,Qiao Chenhui,Zhang Xin,Zhang Weihua,Ma Ning
• Journal of Atherosclerosis and Thrombosis advpub(0), 2015
• … Activating transcription factor 3 (ATF3) is one of the factors involved in regulating the complex process of foam cell formation. … Moreover, ATF3 can act as a negative regulatory factor for inhibiting TN-C-induced foam cell formation by suppressing TLR-4 in LPS-stimulated THP-1 macrophages.Conclusion: ATF3 can inhibit TN-C-induced foam cell formation in LPS-stimulated THP-1 macrophages by suppressing TLR-4. …
• NAID 130005086187

Related Links

• 抗ATF6（Activating Transcription Factor 6）抗体 | 一次抗体 ...

Activating transcription factor 6（ATF6）は，Activator Protein (AP-1 )転写因子のクラスに属する遺伝子で，小胞体（Endoplasmic Reticulum：ER）分子の転写を活性化するERストレスセンサー／トランスデューサーとして機能します。 ATF6 ...

• Activating Transcription Factor 6 - MEDICAL DIAGNOSIS ...

Activating Transcription Factor 6. On-line free medical diagnosis assistant. Ranked list of possible diseases from either several symptoms or a full patient history. A similarity measure between symptoms and diseases is provided.

Related Pictures

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★リンクテーブル★

リンク元	「ATF6」「活性化転写因子6」
関連記事	「fact」「factor」「transcription factor」

「ATF6」

　　[★]

• 活性化転写因子6

関

activating transcription factor 6

「活性化転写因子6」

　　[★]

英

activating transcription factor 6、ATF6

「fact」

　　[★]

• n.

• 事実、現状、実際、実態

関

actual、actually、in fact、in practice、indeed、practically

　 　 　 　 　

「factor」

　　[★]

• n.

• 因子、要因、要素、ファクター

関

element、elementary、factorial、parameter

　 　 　 　 　 　 　

「transcription factor」

　　[★]

• 転写制御因子、転写因子

関

TF、transcriptional regulator、transcriptional regulatory element