Anti-BCL9L Antibody (ARG43189)

Total Page：16

File Type：pdf, Size：1020Kb

Product datasheet [email protected] ARG43189 Package: 50 μg anti-BCL9L antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes BCL9L Tested Reactivity Hu Tested Application ICC, WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name BCL9L Antigen Species Human Immunogen A 20-amino acid peptide within aa. 20-70 of Human BCL9L. Conjugation Un-conjugated Alternate Names Protein BCL9-2; BCL9-2; B-cell CLL/lymphoma 9-like protein; DLNB11; BCL9-like protein; B-cell lymphoma 9-like protein Application Instructions Application table Application Dilution ICC 10 µg/ml WB 1 µg/ml 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 157 kDa Properties Form Liquid Purification Affinity purification with immunogen. Buffer PBS and 0.02% Sodium azide. Preservative 0.02% Sodium azide Concentration 1 mg/ml 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 or below. 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. www.arigobio.com 1/2 Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol BCL9L Gene Full Name B-cell CLL/lymphoma 9-like Function Transcriptional regulator that acts as an activator. Promotes beta-catenin transcriptional activity. Plays a role in tumorigenesis. Enhances the neoplastic transforming activity of CTNNB1 (By similarity). [UniProt] Cellular Localization Nucleus. [UniProt] Images ARG43189 anti-BCL9L antibody ICC image Immunocytochemistry: HeLa cells stained with ARG43189 anti-BCL9L antibody at 10 µg/ml dilution. ARG43189 anti-BCL9L antibody WB image Western blot: HeLa cell lysate stained with ARG43189 anti-BCL9L antibody at 1 µg/ml dilution, in the absence (left) and the presence of blocking peptide (right). www.arigobio.com 2/2 Powered by TCPDF (www.tcpdf.org).

Copy Link

Recommended publications

The Transition from Primary Colorectal Cancer to Isolated Peritoneal Malignancy
medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . The transition from primary colorectal cancer to isolated peritoneal malignancy is associated with a hypermutant, hypermethylated state Sally Hallam1, Joanne Stockton1, Claire Bryer1, Celina Whalley1, Valerie Pestinger1, Haney Youssef1, Andrew D Beggs1 1 = Surgical Research Laboratory, Institute of Cancer & Genomic Science, University of Birmingham, B15 2TT. Correspondence to: Andrew Beggs, [email protected] KEYWORDS: Colorectal cancer, peritoneal metastasis ABBREVIATIONS: Colorectal cancer (CRC), Colorectal peritoneal metastasis (CPM), Cytoreductive surgery and heated intraperitoneal chemotherapy (CRS & HIPEC), Disease free survival (DFS), Differentially methylated regions (DMR), Overall survival (OS), TableFormalin fixed paraffin embedded (FFPE), Hepatocellular carcinoma (HCC) ARTICLE CATEGORY: Research article NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . NOVELTY AND IMPACT: Colorectal peritoneal metastasis (CPM) are associated with limited and variable survival despite patient selection using known prognostic factors and optimal currently available treatments.
[Show full text]
BCL9L and Caspase-2—New Guardians Against Aneuploidy
1142 Editorial BCL9L and caspase-2—new guardians against aneuploidy Narendra Kumar Chunduri, Zuzana Storchova Department of Molecular Genetics, University of Kaiserslautern, Kaiserslautern, Germany Correspondence to: Zuzana Storchova. University of Kaiserslautern, Paul Ehrlich Str. 24, 67663 Kaiserslautern, Germany. Email: [email protected]. Comment on: López-García C, Sansregret L, Domingo E, et al. BCL9L Dysfunction Impairs Caspase-2 Expression Permitting Aneuploidy Tolerance in Colorectal Cancer. Cancer Cell 2017;31:79-93. Submitted Apr 08, 2017. Accepted for publication Aug 18, 2017. doi: 10.21037/tcr.2017.08.37 View this article at: http://dx.doi.org/10.21037/tcr.2017.08.37 Every time cell divides, the chromosomes must be inactivation. In fact, in colorectal cancer (CRC), where duplicated and segregated equally into the two daughter aneuploidy is frequent, p53 inactivation occurs rather late cells. Duplication and segregation of chromosomes is a during tumorigenesis (3). Thus, additional factors might dynamic process that involves highly orchestrated processes guard the cells against aneuploidy and their mutations to ensure faithful transfer of the genetic information. might provide tolerance to chromosome missegregation Infrequently, errors in mitosis can occur that cause the cells irrespective of p53 inactivation. Since aneuploidy is to missegregate one or more chromosomes, which leads considered a promising target for cancer therapy, it is usually to irreversible cell cycle arrest or cell death. In rare of importance to identify the factors that contribute to occasions, some of these cells survive to give rise to daughter aneuploidy tolerance in cancer cells. cells with either loss or gain of chromosomes; a condition In past years, the advent of next generation sequencing known as “aneuploidy”.
[Show full text]
BCL9L Expression in Pancreatic Neoplasia with a Focus on SPN: A
Hallas et al. BMC Cancer (2016) 16:648 DOI 10.1186/s12885-016-2707-1 RESEARCH ARTICLE Open Access BCL9L expression in pancreatic neoplasia with a focus on SPN: a possible explanation for the enigma of the benign neoplasia Cora Hallas* , Julia Phillipp†, Lukas Domanowsky†, Bettina Kah and Katharina Tiemann Abstract Background: Solid pseudopapillary neoplasms of the pancreas (SPN) are rare tumors affecting mainly women. They show an activating mutation in CTNNB1, the gene for β-catenin, and consequently an overactivation of the Wnt/ β-catenin pathway. This signaling pathway is implied in the pathogenesis of various aggressive tumors, including pancreatic adenocarcinomas (PDAC). Despite this, SPN are characterized by an unusually benign clinical course. Attempts to explain this lack of malignancy have led to the discovery of an aberrant expression of the transcription factor FLI1 in SPN. Methods: In 42 primary pancreatic tumors the RNA-expression of the FLI1 targets DKK1, INPP5D, IGFBP3 and additionally two members of the Wnt/β-catenin pathway, namely BCL9 and BCL9L, was investigated using quantitative real time PCR. Expression of these genes was evaluated in SPN (n = 18), PDAC (n = 12) and the less aggressive intraductal papillary mucinous neoplasm IPMN (n = 12) and compared to normal pancreatic tissue. Potential differences between the tumor entities were evaluated using students t-test. Results: The results demonstrated a differential RNA-expression of BCL9L with a lack of expression in SPN (p <0.001), RNA levels similar to normal tissue in IPMN and increased expression in PDAC (p < 0.04). Further, overexpression of the cyclin D1 inhibitor INPP5D in IPMN (p < 0.0001) was found.
[Show full text]
Identification of the Key Genes Implicated in the Transformation of OLP to OSCC Using RNA-Sequencing
ONCOLOGY REPORTS 37: 2355-2365, 2017 Identification of the key genes implicated in the transformation of OLP to OSCC using RNA-sequencing QIAOzHEN YANG1*, BIN GUO2*, HONGYING SUN1, JIE zHANG1, SHANGFENG LIU1, SAIYIN HExIGE2, xUEDI YU1 and xIAxIA WANG1 1Department of Stomatology, Huashan Hospital, Fudan University, Shanghai 200040; 2State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, P.R. China Received August 15, 2016; Accepted January 2, 2017 DOI: 10.3892/or.2017.5487 Abstract. Oral lichen planus (OLP) is a chronic inflammatory downregulated. These findings indicated that BCL9L, GMPS, disease that may transform to oral squamous cell carcinoma HES1, PER2 and TSPAN33 affected the transformation of (OSCC), while its carcinogenesis mechanisms are not entirely OLP to OSCC. clear. This study was designed to identify the important genes involved in the malignant transformation of OLP to OSCC. Introduction After RNA-sequencing, the differently expressed genes (DEGs) in OLP vs. normal and OSCC vs. normal groups, Oral lichen planus (OLP) is a common chronic inflammatory respectively, were identified by limma package in R language, disease of the oral mucosa, which is classified into oral potential and then clustering analysis were conducted by Pheatmap malignant disorders (OPMDs) by World Health Organization package in R language. Weighed gene co-expression network (WHO) (1). OPMD is the general name of diseases occurring analysis (WGCNA) was performed for the DEGs to screen in oral mucosa and with cancerous potential (2). The incidence disease-associated modules. Using Cytoscape software, of OLP is 0.1-4% (3), and its canceration rate is close to 1% (4).
[Show full text]
Human Social Genomics in the Multi-Ethnic Study of Atherosclerosis
Getting “Under the Skin”: Human Social Genomics in the Multi-Ethnic Study of Atherosclerosis by Kristen Monét Brown A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Epidemiological Science) in the University of Michigan 2017 Doctoral Committee: Professor Ana V. Diez-Roux, Co-Chair, Drexel University Professor Sharon R. Kardia, Co-Chair Professor Bhramar Mukherjee Assistant Professor Belinda Needham Assistant Professor Jennifer A. Smith © Kristen Monét Brown, 2017 [email protected] ORCID iD: 0000-0002-9955-0568 Dedication I dedicate this dissertation to my grandmother, Gertrude Delores Hampton. Nanny, no one wanted to see me become “Dr. Brown” more than you. I know that you are standing over the bannister of heaven smiling and beaming with pride. I love you more than my words could ever fully express. ii Acknowledgements First, I give honor to God, who is the head of my life. Truly, without Him, none of this would be possible. Countless times throughout this doctoral journey I have relied my favorite scripture, “And we know that all things work together for good, to them that love God, to them who are called according to His purpose (Romans 8:28).” Secondly, I acknowledge my parents, James and Marilyn Brown. From an early age, you two instilled in me the value of education and have been my biggest cheerleaders throughout my entire life. I thank you for your unconditional love, encouragement, sacrifices, and support. I would not be here today without you. I truly thank God that out of the all of the people in the world that He could have chosen to be my parents, that He chose the two of you.
[Show full text]
Identifying a GSK3-TRARG1 Signaling Axis Reveals BCL9L As a Novel Regulator of GLUT4 Trafficking
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.07.415257; this version posted December 7, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Identifying a GSK3-TRARG1 signaling axis reveals BCL9L as a novel regulator of GLUT4 trafficking Xiaowen Duan1, Dougall M. Norris2, Sean J. Humphrey1, Pengyi Yang3,6, Kristen C. Cooke1, Will P. Bultitude4, Benjamin L. Parker1,a, Olivia J. Conway2, James G. Burchfield1, James R. Krycer1, Frances M. Brodsky4, David E. James1,5♯, Daniel J. Fazakerley1,2♯ 1Charles Perkins Centre, School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW 2006, Australia 2Metabolic Research Laboratories, Wellcome-Medical Research Council Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK 3Charles Perkins Centre, School of Mathematics and Statistics, The University of Sydney, Sydney, NSW 2006, Australia 4Research Department of Structural and Molecular Biology, Division of Biosciences, University College London, Gower Street, London WC1E 6BT, UK 5School of Medicine, The University of Sydney, Sydney, NSW 2006, Australia 6Computational Systems Biology Group, Children’s Medical Research Institute, The University of Sydney, Westmead, NSW 2006, Australia aPresent Address is Department of Physiology, School of Biomedical Sciences, The University of Melbourne, Parkville, VIC, Australia. Corresponding authors: Daniel J. Fazakerley E-mail: [email protected] or David E. James E-mail: [email protected] Running title: TRARG1 is a novel substrate of GSK3 Keywords: glycogen synthase kinase 3 (GSK3), glucose transporter type 4 (GLUT4), trafficking regulator of GLUT4-1 (TRARG1), protein phosphorylation, phosphoproteomics, proteomics, insulin signaling, protein-protein interaction, BCL9L 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.12.07.415257; this version posted December 7, 2020.
[Show full text]
Detection of H3k4me3 Identifies Neurohiv Signatures, Genomic
viruses Article Detection of H3K4me3 Identifies NeuroHIV Signatures, Genomic Effects of Methamphetamine and Addiction Pathways in Postmortem HIV+ Brain Specimens that Are Not Amenable to Transcriptome Analysis Liana Basova 1, Alexander Lindsey 1, Anne Marie McGovern 1, Ronald J. Ellis 2 and Maria Cecilia Garibaldi Marcondes 1,* 1 San Diego Biomedical Research Institute, San Diego, CA 92121, USA; [email protected] (L.B.); [email protected] (A.L.); [email protected] (A.M.M.) 2 Departments of Neurosciences and Psychiatry, University of California San Diego, San Diego, CA 92103, USA; [email protected] * Correspondence: [email protected] Abstract: Human postmortem specimens are extremely valuable resources for investigating trans- lational hypotheses. Tissue repositories collect clinically assessed specimens from people with and without HIV, including age, viral load, treatments, substance use patterns and cognitive functions. One challenge is the limited number of specimens suitable for transcriptional studies, mainly due to poor RNA quality resulting from long postmortem intervals. We hypothesized that epigenomic Citation: Basova, L.; Lindsey, A.; signatures would be more stable than RNA for assessing global changes associated with outcomes McGovern, A.M.; Ellis, R.J.; of interest. We found that H3K27Ac or RNA Polymerase (Pol) were not consistently detected by Marcondes, M.C.G. Detection of H3K4me3 Identifies NeuroHIV Chromatin Immunoprecipitation (ChIP), while the enhancer H3K4me3 histone modification was Signatures, Genomic Effects of abundant and stable up to the 72 h postmortem. We tested our ability to use H3K4me3 in human Methamphetamine and Addiction prefrontal cortex from HIV+ individuals meeting criteria for methamphetamine use disorder or not Pathways in Postmortem HIV+ Brain (Meth +/−) which exhibited poor RNA quality and were not suitable for transcriptional profiling.
[Show full text]
Identification of a Link Between Wnt/Β-Catenin Signalling and the Cell
ARTICLE Received 23 Mar 2011 | Accepted 17 Oct 2011 | Published 22 Nov 2011 DOI: 10.1038/ncomms1551 Identifi cation of a link between Wnt / β -catenin signalling and the cell fusion pathway Ken Matsuura1 , * , Ta k a f u m i J i g a m i 1 , * , Kenzui Taniue1 , Yasuyuki Morishita2 , Shungo Adachi1 , Takao Senda3 , Aya Nonaka 4 , Hiroyuki Aburatani4 , Ts u t o m u N a k a m u r a1 & Tetsu Akiyama1 Cell fusion has a critical role in various developmental processes, immune response, tissue homeostasis and regeneration, and possibly, in cancer. However, the signals that regulate cell fusion remain poorly understood. In a screen for novel targets of Wnt / β -catenin signalling, we identifi ed glial cells missing 1 ( GCM1 ), which encodes a transcription factor that is involved in epigenetic regulation and is critical for the fusion of syncytiotrophoblast (ST) cells. Here we show that β -catenin / BCL9-Like (BCL9L) / T-cell factor 4 (TCF4) signalling directly targets the GCM1 / syncytin pathway and thereby regulates the fusion of human choriocarcinoma cells. Furthermore, we show that the GCM1 / syncytin-B pathway is signifi cantly downregulated in the placenta of BCL9L-defi cient mice and that the fusion and differentiation of ST-II cells are blocked. Our results demonstrate a signal transduction pathway that regulates cell fusion, and may provide intriguing perspectives into the various biological and pathological processes that involve cell fusion. 1 Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo , 1-1-1, Yayoi, Bunkyo-ku, Tokyo 113-0032 , Japan .
[Show full text]
Mutations in Bcl9 and Pygo Genes Cause Congenital Heart Defects by Tissue-Specific Perturbation of Wnt/Β-Catenin Signaling
bioRxiv preprint doi: https://doi.org/10.1101/249680; this version posted January 17, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Mutations in Bcl9 and Pygo genes cause congenital heart defects by tissue-specific perturbation of Wnt/-catenin signaling Claudio Cantù1,†, Anastasia Felker1,†, Dario Zimmerli1,†, Elena Chiavacci1, Elena María Cabello1, Lucia Kirchgeorg1, Tomas Valenta1, George Hausmann1, Jorge Ripoll2, Natalie Vilain3, Michel Aguet3, Konrad Basler1,*, Christian Mosimann1,* 1 Institute of Molecular Life Sciences, University of Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland. 2 Department of Bioengineering and Aerospace Engineering, Universidad Carlos III de Madrid, 28911 Madrid, Spain. 3 Swiss Institute for Experimental Cancer Research (ISREC), École Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, 1015 Lausanne, Switzerland. † contributed equally to this work * correspondence to: [email protected]; [email protected] Abstract Genetic alterations in human BCL9 genes have repeatedly been found in congenital heart disease (CHD) with as-of-yet unclear causality. BCL9 proteins and their Pygopus (Pygo) co-factors can participate in canonical Wnt signaling via binding to β-catenin. Nonetheless, their contributions to vertebrate heart development remain uncharted. Here, combining zebrafish and mouse genetics, we document tissue- specific functions in canonical Wnt signaling for BCL9 and Pygo proteins during heart development. In a CRISPR-Cas9-based genotype-phenotype association screen, we uncovered that zebrafish mutants for bcl9 and pygo genes largely retain β-catenin activity, yet develop cardiac malformations.
[Show full text]
Identification and Interaction Analysis of Molecular Markers in Pancreatic
medRxiv preprint doi: https://doi.org/10.1101/2020.12.20.20248601; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification and Interaction Analysis of Molecular Markers in Pancreatic Ductal Adenocarcinoma by Integrated Bioinformatics Analysis and Molecular Docking Experiments Basavaraj Vastrad1 , Chanabasayya Vastrad *2, Anandkumar Tengli3 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics,Chanabasava Nilaya, Bharthinagar, Dharwad, Karanataka 580001, India. 3. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru and JSS Academy of Higher Education & Research, Mysuru- 570015, Karnataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.20.20248601; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract The current investigation aimed to mine therapeutic molecular targets that play an key part in the advancement of pancreatic ductal adenocarcinoma (PDAC). The expression profiling by high throughput sequencing dataset profile GSE133684 dataset was downloaded from the Gene Expression Omnibus (GEO) database.
[Show full text]
Matrix Stiffness Promotes Glioma Cell Stemness by Activating BCL9L/Wnt/Β-Catenin Signaling
www.aging-us.com AGING 2021, Vol. 13, No. 4 Research Paper Matrix stiffness promotes glioma cell stemness by activating BCL9L/Wnt/β-catenin signaling Bei Tao1,*, Yi Song2,* , Yao Wu2, Xiaobo Yang3,4, Tangming Peng3,4, Lilei Peng3,4, Kaiguo Xia3,4, Xiangguo Xia3,4, Ligang Chen3,4, Chuanhong Zhong3,4 1Department of Rheumatology and Immunology, Affiliated Hospital of Southwest Medical University, Luzhou, China 2Department of Neurosurgery, Chongqing University Three Gorges Hospital, Chongqing, China 3Sichuan Clinic Research Center for Neurosurgery, Luzhou, China 4Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, Luzhou, China *Equal contribution Correspondence to: Chuanhong Zhong; email: [email protected] Keywords: matrix stiffness, glioma, stemness, Wnt/β-catenin Received: July 27, 2020 Accepted: December 9, 2020 Published: February 1, 2021 Copyright: © 2021 Tao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Matrix stiffness is a key physical characteristic of the tumor microenvironment and correlates tightly with tumor progression. Here, we explored the association between matrix stiffness and glioma development. Using atomic force microscopy, we observed higher matrix stiffness in highly malignant glioma tissues than in low- grade/innocent tissues. In vitro and in vivo analyses revealed that culturing glioma cells on stiff polyacrylamide hydrogels enhanced their proliferation, tumorigenesis and CD133 expression. Greater matrix stiffness could obviously up-regulated the expression of BCL9L, thereby promoting the activation of Wnt/β-catenin signaling and ultimately increasing the stemness of glioma cells.
[Show full text]
Nuclear Regulation of Wnt/-Catenin Signaling
G C A T T A C G G C A T genes Review Nuclear Regulation of Wnt/β-Catenin Signaling: It’s a Complex Situation Christin C. Anthony 1 , David J. Robbins 2, Yashi Ahmed 3 and Ethan Lee 1,4,* 1 Department of Cell & Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA; [email protected] 2 Molecular Oncology Program, Division of Surgical Oncology, Dewitt Daughtry Family Department of Surgery, and Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA; [email protected] 3 Department of Molecular and Systems Biology and the Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, NH 03755, USA; [email protected] 4 Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA * Correspondence: [email protected] Received: 14 July 2020; Accepted: 31 July 2020; Published: 4 August 2020 Abstract: Wnt signaling is an evolutionarily conserved metazoan cell communication pathway required for proper animal development. Of the myriad of signaling events that have been ascribed to cellular activation by Wnt ligands, the canonical Wnt/β-catenin pathway has been the most studied and best understood. Misregulation of Wnt/β-catenin signaling has been implicated in developmental defects in the embryo and major diseases in the adult. Despite the latter, no drugs that inhibit the Wnt/β-catenin pathway have been approved by the FDA. In this review, we explore the least understood step in the Wnt/β-catenin pathway—nuclear regulation of Wnt target gene transcription. We initially describe our current understanding of the importation of β-catenin into the nucleus.
[Show full text]