Cyclin A1 Rabbit Pab

Total Page：16

File Type：pdf, Size：1020Kb

Leader in Biomolecular Solutions for Life Science Cyclin A1 Rabbit pAb Catalog No.: A14529 Basic Information Background Catalog No. The protein encoded by this gene belongs to the highly conserved cyclin family, whose A14529 members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct Observed MW expression and degradation patterns which contribute to the temporal coordination of 52kDa each mitotic event. The cyclin encoded by this gene was shown to be expressed in testis and brain, as well as in several leukemic cell lines, and is thought to primarily function in Calculated MW the control of the germline meiotic cell cycle. This cyclin binds both CDK2 and CDC2 47kDa/52kDa kinases, which give two distinct kinase activities, one appearing in S phase, the other in G2, and thus regulate separate functions in cell cycle. This cyclin was found to bind to Category important cell cycle regulators, such as Rb family proteins, transcription factor E2F-1, and the p21 family proteins. Multiple transcript variants encoding different isoforms Primary antibody have been found for this gene. Applications WB Cross-Reactivity Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 8900 P78396 Immunogen A synthetic peptide corresponding to a sequence within amino acids 350-450 of human CCNA1 (NP_001104515.1). Synonyms CCNA1;CT146;cyclin-A1 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using Cyclin A1 antibody (A14529) at 1:3000 dilution. Secondary antibody: HRP Goat Anti-Mouse IgG (H+L) (AS003) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 10s. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

Copy Link

Recommended publications

Insight Into Bortezomib Focusing on Its Efficacy Against P-Gp-Positive
International Journal of Molecular Sciences Article Insight into Bortezomib Focusing on Its Efﬁcacy against P-gp-Positive MDR Leukemia Cells Tomáš Kyca 1, Lucia Pavlíková 1,2, Viera Boháˇcová 1, Anton Mišák 3 , Alexandra Poturnayová 1, Albert Breier 1,4,* , Zdena Sulová 1,* and Mário Šereš 1,2,* 1 Institute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská cesta 9, 84505 Bratislava, Slovakia; [email protected] (T.K.); [email protected] (L.P.); [email protected] (V.B.); [email protected] (A.P.) 2 Institute of Zoology, Slovak Academy of Sciences, Dúbravská cesta 9, 84506 Bratislava, Slovakia 3 Institute for Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 84505 Bratislava, Slovakia; [email protected] 4 Institute of Biochemistry and Microbiology, Faculty of Chemical and Food Technology, Slovak University of Technology in Bratislava, Radlinského 9, 81237 Bratislava 1, Slovakia * Correspondence: [email protected] (A.B.); [email protected] (Z.S.); [email protected] (M.Š.); Tel.: +421-2-593-25-514 or +421-918-674-514 (A.B.); +421-2-3229-5510 (Z.S.) Abstract: In this paper, we compared the effects of bortezomib on L1210 (S) cells with its effects on P-glycoprotein (P-gp)-positive variant S cells, which expressed P-gp either after selection with vincristine (R cells) or after transfection with a human gene encoding P-gp (T cells). Bortezomib induced the death-related effects in the S, R, and T cells at concentrations not exceeding 10 nM.
[Show full text]
TEAD4 Ensures Postimplantation Development by Promoting Trophoblast Self-Renewal: an Implication in Early Human Pregnancy Loss
TEAD4 ensures postimplantation development by promoting trophoblast self-renewal: An implication in early human pregnancy loss Biswarup Sahaa,1,2, Avishek Gangulya,1, Pratik Homea,b, Bhaswati Bhattacharyaa, Soma Raya, Ananya Ghosha, M. A. Karim Rumia,b, Courtney Marshb,c, Valerie A. Frenchc, Sumedha Gunewardenad, and Soumen Paula,b,c,3 aDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160; bInstitute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160; cDepartment of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160; and dDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160 Edited by R. Michael Roberts, University of Missouri, Columbia, MO, and approved June 22, 2020 (received for review February 12, 2020) Early pregnancy loss affects ∼15% of all implantation-confirmed Studies in mutant mouse models showed that failure in pla- human conceptions. However, evolutionarily conserved molecular centation often leads to in utero embryonic death (6, 7). Therefore, mechanisms that regulate self-renewal of trophoblast progenitors impaired placentation due to defective development or function of and their association with early pregnancy loss are poorly under- trophoblast cell lineages is considered one of the major underlying stood. Here, we provide evidence that transcription factor TEAD4 causes of early pregnancy loss. Disruptions of trophoblast pro- ensures survival of postimplantation mouse and human embryos genitor differentiation and defective placentation have also been by controlling self-renewal and stemness of trophoblast progeni- implicated as probable causes of pregnancy-associated compli- tors within the placenta primordium.
[Show full text]
Targeting Cyclin-Dependent Kinase 9 and Myeloid Cell Leukaemia 1 in MYC-Driven B-Cell Lymphoma
Targeting cyclin-dependent kinase 9 and myeloid cell leukaemia 1 in MYC-driven B-cell lymphoma Gareth Peter Gregory ORCID ID: 0000-0002-4170-0682 Thesis for Doctor of Philosophy September 2016 Sir Peter MacCallum Department of Oncology The University of Melbourne Doctor of Philosophy Submitted in total fulfilment of the degree of Abstract Aggressive B-cell lymphomas include diffuse large B-cell lymphoma, Burkitt lymphoma and intermediate forms. Despite high response rates to conventional immuno-chemotherapeutic approaches, an unmet need for novel therapeutic by resistance to chemotherapy and radiotherapy. The proto-oncogene MYC is strategies is required in the setting of relapsed and refractory disease, typified frequently dysregulated in the aggressive B-cell lymphomas, however, it has proven an elusive direct therapeutic target. MYC-dysregulated disease maintains a ‘transcriptionally-addicted’ state, whereby perturbation of A significant body of evidence is accumulating to suggest that RNA polymerase II activity may indirectly antagonise MYC activity. Furthermore, very recent studies implicate anti-apoptotic myeloid cell leukaemia 1 (MCL-1) as a critical survival determinant of MYC-driven lymphoma. This thesis utilises pharmacologic and genetic techniques in MYC-driven models of aggressive B-cell lymphoma to demonstrate that cyclin-dependent kinase 9 (CDK9) and MCL-1 are oncogenic dependencies of this subset of disease. The cyclin-dependent kinase inhibitor, dinaciclib, and more selective CDK9 inhibitors downregulation of MCL1 are used
[Show full text]
Cyclin-Dependent Kinase Control of Motile Ciliogenesis
RESEARCH ARTICLE Cyclin-dependent kinase control of motile ciliogenesis Eszter K Vladar1,2,3*, Miranda B Stratton4, Maxwell L Saal2,3, Glicella Salazar-De Simone5, Xiangyuan Wang6, Debra Wolgemuth6, Tim Stearns4,7, Jeffrey D Axelrod1 1Department of Pathology, Stanford University School of Medicine, Stanford, United States; 2Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Aurora, United States; 3Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, United States; 4Department of Biology, Stanford University, Stanford, United States; 5Center for Radiological Research, Columbia University Medical Center, New York, United States; 6Department of Genetics & Development, Columbia University Medical Center, New York, United States; 7Department of Genetics, Stanford University School of Medicine, Stanford, United States Abstract Cycling cells maintain centriole number at precisely two per cell in part by limiting their duplication to S phase under the control of the cell cycle machinery. In contrast, postmitotic multiciliated cells (MCCs) uncouple centriole assembly from cell cycle progression and produce hundreds of centrioles in the absence of DNA replication to serve as basal bodies for motile cilia. Although some cell cycle regulators have previously been implicated in motile ciliogenesis, how the cell cycle machinery is employed to amplify centrioles is unclear. We use transgenic mice and primary airway epithelial cell culture to show that Cdk2, the kinase responsible for the G1 to S phase transition, is also required in MCCs to initiate motile ciliogenesis. While Cdk2 is coupled with cyclins E and A2 during cell division, cyclin A1 is required during ciliogenesis, contributing to an *For correspondence: alternative regulatory landscape that facilitates centriole amplification without DNA replication.
[Show full text]
Upregulation of CDKN2A and Suppression of Cyclin D1 Gene
European Journal of Endocrinology (2010) 163 523–529 ISSN 0804-4643 CLINICAL STUDY Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas Yuji Tani, Naoko Inoshita1, Toru Sugiyama, Masako Kato, Shozo Yamada2, Masayoshi Shichiri3 and Yukio Hirata Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan, Departments of 1Pathology and 2Hypothalamic and Pituitary Surgery, Toranomon Hospital, Tokyo 105-8470, Japan and 3Department of Endocrinology, Diabetes and Metabolism, School of Medicine, Kitasato University, Kanagawa 252-0375, Japan (Correspondence should be addressed to Y Hirata; Email: [email protected]) Abstract Objective: Cushing’s disease (CD) is usually caused by ACTH-secreting pituitary microadenomas, while silent corticotroph adenomas (SCA) are macroadenomas without Cushingoid features. However, the molecular mechanism(s) underlying their different tumor growth remains unknown. The aim of the current study was to evaluate and compare the gene expression proﬁle of cell cycle regulators and cell growth-related transcription factors in CD, SCA, and non-functioning adenomas (NFA). Design and methods: Tumor tissue specimens resected from 43 pituitary tumors were studied: CD (nZ10), SCA (nZ11), and NFA (nZ22). The absolute transcript numbers of the following genes were quantiﬁed with real-time quantitative PCR assays: CDKN2A (or p16INK4a), cyclin family (A1, B1, D1, and E1), E2F1, RB1, BUB1, BUBR1, ETS1, and ETS2. Protein expressions of p16 and cyclin D1 were semi-quantitatively evaluated by immunohistochemical study. Results and conclusion: CDKN2A gene expression was about fourfold greater in CD than in SCA and NFA.
[Show full text]
The Combined Detection of Amphiregulin, Cyclin A1 and DDX20/Gemin3 Expression Predicts Aggressive Forms of Oral Squamous Cell Carcinoma
British Journal of Cancer www.nature.com/bjc ARTICLE OPEN Molecular Diagnostics The combined detection of Amphiregulin, Cyclin A1 and DDX20/Gemin3 expression predicts aggressive forms of oral squamous cell carcinoma 1 2 3 1 1 1 1 Ekaterina Bourova-Flin✉, Samira Derakhshan , Afsaneh✉ Goudarzi , Tao Wang , Anne-Laure Vitte , Florent Chuffart , Saadi Khochbin , Sophie Rousseaux 1 and Pouyan Aminishakib 2,4 © The Author(s) 2021 BACKGROUND: Large-scale genetic and epigenetic deregulations enable cancer cells to ectopically activate tissue-specific expression programmes. A specifically designed strategy was applied to oral squamous cell carcinomas (OSCC) in order to detect ectopic gene activations and develop a prognostic stratification test. METHODS: A dedicated original prognosis biomarker discovery approach was implemented using genome-wide transcriptomic data of OSCC, including training and validation cohorts. Abnormal expressions of silent genes were systematically detected, correlated with survival probabilities and evaluated as predictive biomarkers. The resulting stratification test was confirmed in an independent cohort using immunohistochemistry. RESULTS: A specific gene expression signature, including a combination of three genes, AREG, CCNA1 and DDX20, was found associated with high-risk OSCC in univariate and multivariate analyses. It was translated into an immunohistochemistry-based test, which successfully stratified patients of our own independent cohort. DISCUSSION: The exploration of the whole gene expression profile characterising
[Show full text]
Targeting Cyclin-Dependent Kinases in Human Cancers: from Small Molecules to Peptide Inhibitors
Cancers 2015, 7, 179-237; doi:10.3390/cancers7010179 OPEN ACCESS cancers ISSN 2072-6694 www.mdpi.com/journal/cancers Review Targeting Cyclin-Dependent Kinases in Human Cancers: From Small Molecules to Peptide Inhibitors Marion Peyressatre †, Camille Prével †, Morgan Pellerano and May C. Morris * Institut des Biomolécules Max Mousseron, IBMM-CNRS-UMR5247, 15 Av. Charles Flahault, 34093 Montpellier, France; E-Mails: [email protected] (M.P.); [email protected] (C.P.); [email protected] (M.P.) † These authors contributed equally to this work. * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +33-04-1175-9624; Fax: +33-04-1175-9641. Academic Editor: Jonas Cicenas Received: 17 December 2014 / Accepted: 12 January 2015 / Published: 23 January 2015 Abstract: Cyclin-dependent kinases (CDK/Cyclins) form a family of heterodimeric kinases that play central roles in regulation of cell cycle progression, transcription and other major biological processes including neuronal differentiation and metabolism. Constitutive or deregulated hyperactivity of these kinases due to amplification, overexpression or mutation of cyclins or CDK, contributes to proliferation of cancer cells, and aberrant activity of these kinases has been reported in a wide variety of human cancers. These kinases therefore constitute biomarkers of proliferation and attractive pharmacological targets for development of anticancer therapeutics. The structural features of several of these kinases have been elucidated and their molecular mechanisms of regulation characterized in depth, providing clues for development of drugs and inhibitors to disrupt their function. However, like most other kinases, they constitute a challenging class of therapeutic targets due to their highly conserved structural features and ATP-binding pocket.
[Show full text]
Differential Expression of Cell Cycle Regulators in CDK5- Dependent Medullary Thyroid Carcinoma Tumorigenesis
www.impactjournals.com/oncotarget/ Oncotarget, Vol. 6, No. 14 Differential expression of cell cycle regulators in CDK5- dependent medullary thyroid carcinoma tumorigenesis Karine Pozo1, Antje Hillmann1, Alexander Augustyn2,3, Florian Plattner1, Tao Hai4, Tanvir Singh1, Saleh Ramezani5, Xiankai Sun5, Roswitha Pfragner6, John D. Minna2,3,7, Gilbert J. Cote4, Herbert Chen8, James A. Bibb1,5,9,* and Fiemu E. Nwariaku10,* 1 Department of Psychiatry, The University of Texas Southwestern Medical Center, Dallas, TX, USA 2 Hamon Center for Therapeutic Oncology Research, The University of Texas Southwestern Medical Center, Dallas, TX, USA 3 Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, TX, USA 4 Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 5 Department of Radiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA 6 Institute of Pathophysiology and Immunology, Medical University of Graz, Graz, Austria 7 Department of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, TX, USA 8 Endocrine Surgery Research Laboratory, The University of Wisconsin Carbone Cancer Center, Madison, WI, USA 9 Department of Neurology and Neurotherapeutics, The University of Texas Southwestern Medical Center, Dallas, TX, USA 10 Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX, USA * These authors have contributed equally to this work Correspondence to: James A. Bibb, email: [email protected] Correspondence to :Karine Pozo, email: [email protected] Keywords: Cdk5, retinoblastoma protein, neuroendocrine, medullary thyroid carcinoma, cell cycle Received: August 26, 2014 Accepted: March 03, 2015 Published: April 14, 2015 This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
[Show full text]
Effects of Flavonoids on Expression of Genes Involved in Cell Cycle
Mol Cell Biochem (2015) 407:97–109 DOI 10.1007/s11010-015-2458-3 Effects of flavonoids on expression of genes involved in cell cycle regulation and DNA replication in human fibroblasts 1 2 2 Marta Moskot • Joanna Jako´bkiewicz-Banecka • Elwira Smolin´ska • 2 2 1 Ewa Piotrowska • Grzegorz We˛grzyn • Magdalena Gabig-Cimin´ska Received: 16 January 2015 / Accepted: 16 May 2015 / Published online: 24 May 2015 Ó The Author(s) 2015. This article is published with open access at Springerlink.com Abstract Flavonoids have been studied as potential accompanied by activation of CDKN1A, CDKN1C, agents in medicine for many years. Among them, genistein CDKN2A, CDKN2B, CDKN2C, and GADD45A genes, as was found to be active in various biological systems, well as down-regulation of several mRNAs specific for this mainly in prevention of cancer. Our recent work supported stage, demonstrated by transcriptomic assessments. We the idea that genistein also impacts multiple cellular pro- believe that studies described in this paper will be helpful cesses in healthy fibroblasts; however, its effects on cell in elucidating molecular mechanisms of action of genistein cycle-related pathways remained to be elucidated. Thus, in as modulator of cell cycle and inhibitor of DNA replication this work, high throughput screening with microarrays in humans. coupled to real-time quantitative Reverse Transcription PCR analyses was employed to study the changes in ex- Keywords Flavonoids Á Cell cycle regulation Á DNA pression of key genes associated with cell cycle regulation replication process Á Gene expression profiling Á Cell and/or DNA replication in response to genistein, growth kaempferol, daidzein, and mixtures of genistein and either kaempferol or daidzein.
[Show full text]
Gene Section Review
Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST -CNRS Gene Section Review CCNA1 (cyclin A1) Immacolata Vocca, Gianmarco Muzi, Francesca Pentimalli, Antonio Giordano INT-CROM, National Cancer Institute, 'Pascale Foundation', - Cancer Research Center, Via Ammiraglio Bianco 83013, Mercogliano, Avellino, Italy (IV, FP), Department of Human Pathology and Oncology, University of Siena, Siena, Italy (GM), INT-CROM, National Cancer Institute, 'Pascale Foundation', - Cancer Research Center, Via Ammiraglio Bianco 83013, Mercogliano, Avellino, Italy; Department of Human Pathology and Oncology, University of Siena, Siena, Italy; Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University Philadelphia, PA, USA (AG) Published in Atlas Database: May 2012 Online updated version : http://AtlasGeneticsOncology.org/Genes/CCNA1ID949ch13q13.html DOI : 10.4267/2042/48223 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2012 Atlas of Genetics and Cytogenetics in Oncology and Haematology does not possess a TATA box, whereas the region Identity upstream of the transcriptional start site region contains HGNC (Hugo): CCNA1 four GC boxes, with multiple Sp1-binding sites Location: 13q13.3 important for the regulation of cyclin A1 expression (Müller et al., 1999). Three different transcript variants exist: isoform "a" is DNA/RNA the longest transcript and encodes the longest isoform; Description isoform "b" has an alternate in-frame splice site in the 5' coding region resulting in a protein that is 1 amino The CCNA1 gene is located at chromosome 13q12.3- acid shorter than isoform "a"; isoform "c" contains a q13 (Yang et al., 1997) and made up of 9 exons and 8 distinct 5' UTR and lacks an in-frame portion of the 5' introns that extend over ~ 13 kb (Müller et al., 1999).
[Show full text]
Anti-Cyclin A1 + Cyclin A2 Antibody (ARG41929)
Product datasheet [email protected] ARG41929 Package: 100 μl anti-Cyclin A1 + Cyclin A2 antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes Cyclin A1 + Cyclin A2 Tested Reactivity Hu Tested Application IHC-P, IP, WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name Cyclin A1 + Cyclin A2 Antigen Species Human Immunogen Synthetic peptide of Human Cyclin A1/A2. Conjugation Un-conjugated Alternate Names Cyclin A1: CT146; Cyclin-A1 Cyclin A2: Cyclin-A2; Cyclin-A; CCN1; CCNA Application Instructions Application table Application Dilution IHC-P 1:100 - 1:500 IP 1:50 WB 1:500 - 1:1000 Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Positive Control HeLa Calculated Mw Cyclin A1: 52 kDa Cyclin A2: 49 kDa Observed Size ~ 53 kDa Properties Form Liquid Purification Affinity purified. Buffer PBS (pH 7.4), 150 mM NaCl, 0.02% Sodium azide and 50% Glycerol. Preservative 0.02% Sodium azide Stabilizer 50% Glycerol www.arigobio.com 1/3 Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol CCNA1; CCNA2 Gene Full Name cyclin A1; cyclin A2 Background Cyclin A1: The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle.
[Show full text]
The AP-1 Transcription Factor Regulates Breast Cancer Cell Growth Via Cyclins and E2F Factors
Oncogene (2008) 27, 366–377 & 2008 Nature Publishing Group All rights reserved 0950-9232/08 $30.00 www.nature.com/onc ORIGINAL ARTICLE The AP-1 transcription factor regulates breast cancer cell growth via cyclins and E2F factors Q Shen, IP Uray, Y Li, TI Krisko, TE Strecker, H-T Kim and PH Brown Breast Center, Departments of Medicine and Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA The activating protein-1 (AP-1) transcription factor Introduction transduces growth signals through signal transduction pathways to the nucleus, leading to the expression of genes The activating protein-1 (AP-1) family of transcription involved in growth and malignant transformation in many factors consists of multiple Jun (cJun, JunB and JunD) cell types. We have previously shown that overexpression and Fos (cFos, FosB, Fra-1 and Fra-2) members (Angel of a dominant negative form of the cJun proto-oncogene, a and Karin, 1991). The Jun members either homodimer- cJun dominant negative mutant (Tam67), blocks AP-1 ize with Jun itself or heterodimerize with different Fos transcriptional activity, induces a G1 cell cycle block and members, whereas Fos members heterodimerize only inhibits breast cancer cell growth in vitro and in vivo.We with Jun members. Thus, Jun is the predominant found that AP-1 blockade byTam67 in MCF-7 breast partner to form AP-1 complexes such as Jun:Jun or cancer cells downregulates cyclin D1 transcriptional Jun:Fos dimers. The AP-1 complex converges multiple activitybyat least two mechanisms: bysuppressing trans- growth signals at the transcriptional level, making it a cription at the known AP-1 binding site (À934/À928) critical connecting node for many signal transduction and bysuppressing growth factor-induced expression pathways.
[Show full text]