transcription factor AP-1

転写因子AP-1

関

activator protein-1、AP-1

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. the 1st letter of the Roman alphabet (同)a
15. the blood group whose red cells carry the A antigen (同)type_A, group A

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)
4. answer / ampere
5. antipersonnel / (またA.P.)Associated Press

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/10/18 09:21:20」(JST)

wiki en

[Wiki en表示]

AP-1/DNA complex. Crystallographic structure (PDB 1FOS) of the AP-1 heterodimer comprising c-Fos (cyan) and c-Jun (green) complexed with DNA (brown).

In the field of molecular biology, the activator protein 1 (AP-1) is a transcription factor which is a heterodimeric protein composed of proteins belonging to the c-Fos, c-Jun, ATF and JDP families. It regulates gene expression in response to a variety of stimuli, including cytokines, growth factors, stress, and bacterial and viral infections. AP-1 in turn controls a number of cellular processes including differentiation, proliferation, and apoptosis.

AP-1 upregulates transcription of genes containing the TPA DNA response element (TRE; 5'-TGAG/CTCA-3'). AP-1 binds to this DNA sequence via a basic amino acid region, while the dimeric structure is formed by a leucine zipper.　

Regulome

See also

• Activator protein

References

External links

• NLM
• Genecards
• Atlas of Genetics

UpToDate Contents

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• 1. 喘息における吸入ステロイドの分子学的影響molecular effects of inhaled glucocorticoid therapy in asthma [show details]
  …molecule (eg, CREB-binding protein) binds to a proinflammatory transcription factor (eg, nuclear factor-kappa B [NF-kB], activator protein-1 [AP-1]). The coactivator molecule then acetylates core histones, …
• 2. T細胞受容体シグナル伝達t cell receptor signaling [show details]
  …Downstream from these events, there is activation of transcription factors, such as nuclear factor of activated T cells (NF-AT), activator protein 1 (AP-1), and nuclear factor kappa light-chain enhancer of …
• 3. 喘息におけるステロイド耐性のメカニズムおよび 臨床的意義mechanisms and clinical implications of glucocorticoid resistance in asthma [show details]
  …pro-inflammatory transcription factor activator protein (AP)-1 was significantly reduced in GC-resistant patients, although interaction with NF-kappaB was unaffected . An increase in the basal levels of AP-1 DNA binding …
• 4. 慢性関節リウマチにおける滑膜異常synovial pathology in rheumatoid arthritis [show details]
  …understanding the role of transcription factors in the pathogenesis of RA, especially since they are potential targets for therapeutic intervention. The AP-1 family of transcription factors (c-Jun, c-Fos, JunB …
• 5. 常染色体優性多発性嚢胞腎の遺伝学および嚢胞成長のメカニズムgenetics of autosomal dominant polycystic kidney disease and mechanisms of cyst growth [show details]
  …the polycystin complex has not been identified . However, polycystin-1 can modify activator protein-1 transcription factors, which are involved in the regulation of cell proliferation and survival . The PKD2 …

English Journal

• EBV-Encoded LMP-1 Sensitizes Nasopharyngeal Carcinoma Cells to Genotoxic Drugs by Down-Regulating Cabin1 Expression.

• Chang PY, Wu ZZ, Sun NK, Chao CC.Author information Tumor Biology Laboratory, Department of Biochemistry and Molecular Biology, Chang Gung University College of Medicine, Gueishan, Taoyuan, Taiwan, Republic of China.AbstractThe oncogenic latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) is involved in the pathogenesis of human nasopharyngeal carcinoma (NPC) and lymphoma. We and other authors have shown earlier that LMP1 induces apoptosis and inhibits xenograft tumor growth in mice, but the mechanism underlying these processes has not been investigated so far. In the present study, we show that knockdown of LMP1 renders the EBV-positive NPC cell line CG-1 resistant to various genotoxic drugs (cisplatin, etoposide, and adriamycin). LMP1 inhibits the expression of Cabin1, a Ca(2+) regulated protein shown earlier to inhibit calcineurin. Knockdown of calcineurin binding protein (Cabin1) with small hairpin RNA sensitizes CG-1 cells to genotoxic drugs. In contrast, LMP1 overexpression reduces Cabin1 level and renders both CG-1 cells and EBV-negative NPC cell lines sensitive to cisplatin. The c-Jun-N-terminal kinase (JNK) and ERK pathways are required for LMP1-induced suppression of Cabin1 at the transcriptional level. Chromatin immunoprecipitation assays further confirm that the JNK-activated transcription factor AP-1 mediates the LMP1-induced down-regulation of Cabin1 gene expression. LMP1 knockdown also increases the resistance of xenograph tumors to cisplatin in mice, therefore confirming the relevance of our findings in vivo. This study reveals the molecular mechanism underlying the pro-apoptotic activity of LMP1 during cisplatin-based NPC chemotherapy. J. Cell. Physiol. 229: 309-322, 2014. © 2013 Wiley Periodicals, Inc.
• Journal of cellular physiology.J Cell Physiol.2014 Mar;229(3):309-22. doi: 10.1002/jcp.24448.
• The oncogenic latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) is involved in the pathogenesis of human nasopharyngeal carcinoma (NPC) and lymphoma. We and other authors have shown earlier that LMP1 induces apoptosis and inhibits xenograft tumor growth in mice, but the mechanism underlyi
• PMID 23939952

• Macrophage polarization and function with emphasis on the evolving roles of coordinated regulation of cellular signaling pathways.

• Zhou D1, Huang C1, Lin Z1, Zhan S1, Kong L1, Fang C2, Li J3.Author information 1School of Pharmacy, Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei 230032, China; Institute for Liver Diseases of Anhui Medical University (AMU), Anhui Medical University, Hefei 230032, China.2School of Pharmacy, Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei 230032, China; Department of Ophthalmology, The 1st Affiliated Hospital of Anhui Medical University, Hefei, China.3School of Pharmacy, Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei 230032, China; Institute for Liver Diseases of Anhui Medical University (AMU), Anhui Medical University, Hefei 230032, China. Electronic address: lj@ahmu.edu.cn.AbstractMonocytes/macrophages are heterogeneous and versatile cells that could undergo their phenotypically/functionally dynamic switch in response to the microenvironment signals. Two major macrophage subpopulations with different functions which represent extreme of a continuum in a universe of activation states, including classically activated/inflammatory (M1) and alternatively activated/regenerative (M2) macrophages, have long been recognized. Emerging evidence through genetic or pharmacologic approaches has now been made in defining the actual fate in vivo and in vitro underlying M1 or M2-like polarized activation under physiological and pathological conditions. These cells are characterized by their expression of cell surface markers, secreted cytokines and chemokines, and transcription and epigenetic pathways. Here in this review, we shed new light on the contribution of several major signaling pathways and their modulators/targets involved in directing the macrophage plasticity and polarized function, assess the mechanisms of macrophage polarization by interacting endogenous cellular mechanisms and molecules associated with reciprocal skewing of macrophage polarization between the M1 and M2 states. The identification of mechanisms underlying functional polarization of macrophages into M1 or M2 cells might provide new insights into a basis for macrophage-centered diagnostic and therapeutic strategies for multiple diseases.
• Cellular signalling.Cell Signal.2014 Feb;26(2):192-7. doi: 10.1016/j.cellsig.2013.11.004. Epub 2013 Nov 9.
• Monocytes/macrophages are heterogeneous and versatile cells that could undergo their phenotypically/functionally dynamic switch in response to the microenvironment signals. Two major macrophage subpopulations with different functions which represent extreme of a continuum in a universe of activation
• PMID 24219909

• Increased activity of mitogen activated protein kinase pathway in flotillin-2 knockout mouse model.

• Banning A1, Regenbrecht CR2, Tikkanen R3.Author information 1Institute of Biochemistry, Medical Faculty, University of Giessen, Friedrichstrasse 24, 35392 Giessen, Germany.2Institute for Pathology & LFGC, Charité, University Hospital Berlin, Charitéplatz 1, Berlin, Germany.3Institute of Biochemistry, Medical Faculty, University of Giessen, Friedrichstrasse 24, 35392 Giessen, Germany. Electronic address: Ritva.Tikkanen@biochemie.med.uni-giessen.de.AbstractFlotillins are highly conserved and widely spread proteins that function in receptor tyrosine kinase signaling and membrane trafficking processes. Flotillin-1 and flotillin-2 have been shown to form both homo- and hetero-oligomers, and their cellular localization changes during signaling. Increased expression of flotillins has been detected in several types of cancer and shown to correlate with poor survival. Consistently, flotillin-2 knockout mice show a reduced formation of metastases in a breast cancer animal model. Our recent data have shown that flotillin-1 depletion results in diminished activation of the epidermal growth factor receptor and impairs its downstream signaling towards the mitogen activated protein kinases and the respective transcriptional response. Here we show that genetic ablation of flotillin-2 in a mouse model or its knockdown in cultured cells increases extracellular signal regulated kinase (ERK) activation. Furthermore, the downstream transcriptional targets of ERK and p53 are upregulated at both mRNA and protein levels. These data suggest that opposite effects are obtained upon ablation of one of the two flotillins, with flotillin-2 knockout/knockdown enhancing and flotillin-1 knockdown inhibiting ERK signaling. Due to their overexpression in cancers, flotillins may be considered as cancer therapy targets. However, our findings suggest that care needs to be taken when interfering with flotillin function, as undesired effects such as deregulation of growth-associated genes may emerge in certain cell types.
• Cellular signalling.Cell Signal.2014 Feb;26(2):198-207. doi: 10.1016/j.cellsig.2013.11.001. Epub 2013 Nov 9.
• Flotillins are highly conserved and widely spread proteins that function in receptor tyrosine kinase signaling and membrane trafficking processes. Flotillin-1 and flotillin-2 have been shown to form both homo- and hetero-oligomers, and their cellular localization changes during signaling. Increased
• PMID 24216609

Japanese Journal

• Journal of Health Science

• Kim Ki Mo,Im A-Rang,Park Se Kyu,Shin Hyoung Seok,Chae Sung-wook
• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 42(9), 1524-1531, 2019
• … Similarly, TA-III inhibited UVB-induced cyclooxygenase-2 (COX-2), matrix metalloproteinase-9 (MMP-9) transcription level and protein expression in a dose-dependent manner at non-cytotoxic dose. …
• NAID 130007700090

• JunB regulates homeostasis and suppressive functions of effector regulatory T cells

• Shin-ichi Koizumi,Daiki Sasaki,Tsung-Han Hsieh,Naoyuki Taira,Nana Arakaki,Shinichi Yamasaki,Ke Wang,Shukla Sarkar,Hiroki Shirahata,Mio Miyagi,Hiroki Ishikawa
• Nature Communications 9(1), 5344, 2018-12-17
• … T-cell receptor (TCR)-dependent induction of the transcription factor IRF4 is essential for eTreg differentiation, but how IRF4 activity is regulated in Treg cells is still unclear. … Here we show that the AP-1 transcription factor, JunB, is expressed in eTreg cells and promotes an IRF4-dependent transcription program. …
• NAID 120006645276

• AP-1転写因子JunBによるTh17細胞分化の制御

• 山﨑 創
• 臨床免疫・アレルギー科 = Clinical immunology & allergology 70(3), 275-282, 2018-09
• NAID 40021674531

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★リンクテーブル★

リンク元	「activator protein-1」「転写因子AP-1」
関連記事	「AP」「fact」「factor」「transcription factor」「A」

「activator protein-1」

　　[★]

アクチベータータンパク質1

関

AP-1、transcription factor AP-1

「転写因子AP-1」

　　[★]

英

transcription factor AP-1

関

アクチベータータンパク質1

「AP」

　　[★]

• 狭心症 angina pectoris,
• アルカリホスファターゼ alkaline phosphatase
• 活動電位 action potential
• アクチベーター蛋白質 activator protein
• アミノプリン aminopurine
• 順行性腎盂造影 antegrade pyelography

　

「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

「A」

　　[★]

• アデニン adenine
• アデノシン adenosine
• アラニン alanine