HOXA6 Antibody (Center) Blocking Peptide Synthetic Peptide Catalog # Bp12025c

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HOXA6 Antibody (Center) Blocking Peptide Synthetic Peptide Catalog # Bp12025c

10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 HOXA6 Antibody (Center) Blocking peptide Synthetic peptide Catalog # BP12025c Specification HOXA6 Antibody (Center) Blocking HOXA6 Antibody (Center) Blocking peptide - peptide - Background Product Information In vertebrates, the genes encoding the class Primary Accession P31267 oftranscription factors called homeobox genes are found in clustersnamed A, B, C, and D on four separate chromosomes. Expression HOXA6 Antibody (Center) Blocking peptide - Additional Information ofthese proteins is spatially and temporally regulated duringembryonic development. This gene is part of the A cluster onchromosome 7 Gene ID 3203 and encodes a DNA-binding transcription factor whichmay regulate gene expression, Other Names morphogenesis, and differentiation. Homeobox protein Hox-A6, Homeobox protein Hox-1B, HOXA6, HOX1B HOXA6 Antibody (Center) Blocking peptide - References Format Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in Yerges, L.M., et al. J. Bone Miner. Res. solution using the appropriate buffer as 24(12):2039-2049(2009)Dickson, G.J., et al. needed. Exp. Hematol. 37(3):322-333(2009)Lamesch, P., et al. Genomics 89(3):307-315(2007)Kosaki, Storage K., et al. Teratology 65(2):50-62(2002)Walters, Maintain refrigerated at 2-8°C for up to 6 J.R., et al. Gastroenterology months. For long term storage store at 113(2):472-477(1997) -20°C. Precautions This product is for research use only. Not for use in diagnostic or therapeutic procedures. HOXA6 Antibody (Center) Blocking peptide - Protein Information Name HOXA6 Synonyms HOX1B Function Sequence-specific transcription factor which is part of a developmental regulatory system that provides cells with specific positional identities on the anterior-posterior axis. Cellular Location Nucleus. Page 1/2 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 HOXA6 Antibody (Center) Blocking peptide - Protocols Provided below are standard protocols that you may find useful for product applications. • Blocking Peptides Page 2/2 Powered by TCPDF (www.tcpdf.org).

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Homeobox Gene Methylation in Lung Cancer Studied by Genome-Wide Analysis with a Microarray-Based Methylated Cpg Island Recovery Assay
Homeobox gene methylation in lung cancer studied by genome-wide analysis with a microarray-based methylated CpG island recovery assay Tibor Rauch*, Zunde Wang*, Xinmin Zhang†, Xueyan Zhong*, Xiwei Wu‡, Sean K. Lau§, Kemp H. Kernstine¶, Arthur D. Riggs*ʈ, and Gerd P. Pfeifer*ʈ *Division of Biology, ‡Division of Information Sciences, §Division of Pathology, and ¶Division of Surgery, Beckman Research Institute of the City of Hope, Duarte, CA 91010; and †NimbleGen Systems, Inc., Madison, WI 53711 Contributed by Arthur D. Riggs, February 5, 2007 (sent for review December 11, 2006) De novo methylation of CpG islands is a common phenomenon in and in this way they are key determinants of cell identity and human cancer, but the mechanisms of cancer-associated DNA potential targets during tumorigenesis. methylation are not known. We have used tiling arrays in combi- We recently developed a DNA methylation detection technique, nation with the methylated CpG island recovery assay to investi- the methylated CpG island recovery assay (MIRA) (12). This gate methylation of CpG islands genome-wide and at high reso- technique is based on the high affinity of a complex of the MBD2b lution. We ﬁnd that all four HOX gene clusters on chromosomes 2, and MBD3L1 proteins for CpG-methylated DNA (13) and is 7, 12, and 17 are preferential targets for DNA methylation in cancer compatible with microarray-based methodology (14). We previ- cell lines and in early-stage lung cancer. CpG islands associated ously found that several homeobox genes were methylated in a lung with many other homeobox genes, such as SIX, LHX, PAX, DLX, and cancer cell line (14).
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Continuous MLL-ENL Expression Is Necessary to Establish a ''Hox Code'' and Maintain Immortalization of Hematopoietic Progenitor Cells
Research Article Continuous MLL-ENL Expression Is Necessary to Establish a ‘‘Hox Code’’ and Maintain Immortalization of Hematopoietic Progenitor Cells Sarah J. Horton,1 David G. Grier,3 Glenda J. McGonigle,3 Alexander Thompson,3 Michelle Morrow,1 Inusha De Silva,1 Dale A. Moulding,1 Dimitris Kioussis,2 Terence R.J. Lappin,3 Hugh J.M. Brady,1 and Owen Williams1 1Molecular Haematology and Cancer Biology Unit, Institute of Child Health, University College London; 2Division of Molecular Immunology, National Institute for Medical Research, London, United Kingdom; and 3Department of Child Health, Queen’s University, Belfast, United Kingdom Abstract essential for definitive hematopoiesis and that it is required to The t[(11;19)(p22;q23)] translocation, which gives rise to the maintain, but not to initiate, the expression of multiple Hox genes MLL-ENL fusion protein, is commonly found in infant acute during embryogenesis (5–9). Some Hox genes are oncogenic when leukemias of both the myeloid and lymphoid lineage. To overexpressed in hematopoietic progenitor cells (10, 11). Taken investigate the molecular mechanism of immortalization by together, this suggests that aberrant regulation of Hox genes by MLL-ENL we established a Tet-regulatable system of MLL- MLL fusion proteins is the basis for leukemias involving MLL ENL expression in primary hematopoietic progenitor cells. translocations (12). Several recent publications do indeed suggest Immortalized myeloid cell lines were generated, which that Hox genes may play an important role in leukemia induced by are dependent on continued MLL-ENL expression for their MLL fusion proteins (13–16). survival and proliferation. These cells either terminally MLL translocations result in the generation of an in-frame differentiate or die when MLL-ENL expression is turned chimeric fusion in which MLL is joined to one of over 40 different off with doxycycline.
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Rabbit Anti-HOXA6/FITC Conjugated Antibody
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Inactivation of HOXA Genes by Hypermethylation in Myeloid and Lymphoid Malignancy Is Frequent and Associated with Poor Prognosis Gordon Strathdee,1Tessa L
Imaging, Diagnosis, Prognosis Inactivation of HOXA Genes by Hypermethylation in Myeloid and Lymphoid Malignancy is Frequent and Associated with Poor Prognosis Gordon Strathdee,1Tessa L. Holyoake,2 Alyson Sim,1Anton Parker,4 David G. Oscier,4 Junia V. Melo, 5 Stefan Meyer,6,7 Tim Eden,7 Anne M. Dickinson,8 Joanne C. Mountford,2 Heather G. Jorgensen,2 Richard Soutar, 3 and Robert Brown1 Abstract Purpose: The HOX genes comprise a large family of homeodomain-containing transcription factors, present in four separate clusters, which are key regulators of embryonic development, hematopoietic differentiation, and leukemogenesis. We aimed to study the role of DNA methyl- ation as an inducer of HOX gene silencing in leukemia. Experimental Design: Three hundred and seventy-eight samples of myeloid and lymphoid leukemia were quantitatively analyzed (by COBRA analysis and pyrosequencing of bisulfite- modified DNA) for methylation of eight HOXA and HOXB cluster genes. The biological significance of the methylation identified was studied by expression analysis and through re-expression of HOXA5 in a chronic myeloid leukemia (CML) blast crisis cell line model. Results: Here, we identify frequent hypermethylation and gene inactivation of HOXA and HOXB cluster genes in leukemia. In particular, hypermethylation of HOXA4 and HOXA5 was frequently observed (26-79%) in all types of leukemias studied. HOXA6 hypermethylation was predomi- nantly restricted to lymphoid malignancies, whereas hypermethylation of other HOXA and HOXB genes was only observed in childhood leukemia. HOX gene methylation exhibited clear correla- tions with important clinical variables, most notably in CML, in which hypermethylation of both HOXA5 (P = 0.00002) and HOXA4 (P = 0.006) was strongly correlated with progression to blast crisis.
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A Review of Epigenetic and Gene Expression Alterations Associated with Intracranial Meningiomas
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“Indeed, the Homeobox Has Been Called the 'Rosetta Stone' Of
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Class Discovery in Acute Lymphoblastic Leukemia Using Gene Expression Analysis
Class Discovery in Acute Lymphoblastic Leukemia using Gene Expression Analysis Uri Einav M.Sc. Thesis submitted to the Scientific Council of the Weizmann Institute of Science Research conducted under the supervision of Prof. Eytan Domany December 2003 Acknowledgements I would like to express my sincere gratitude to my supervisor, Professor Eytan Domany, for his continuous fascinating guidance, advice and support throughout the course of this research. I also wish to thank Professor Gideon Rechavi and Dr. Ninette Amariglio for their enlightening discussions. I am grateful to the members of 'Domany's group' and especially to Omer Barad, Gaddy Getz and Yuval Tabach for fruitful discussions. My deep gratitude goes to my family and particularly to Yael for their encouragement. Contents ABSTRACT 2 1 INTRODUCTION 3 1.1 LEUKEMIA 3 1.2 SUBTYPES OF LEUKEMIA 4 1.3 ETIOLOGY OF CHILDHOOD LEUKEMIA 7 1.4 THE IMPORTANCE OF CLASS DISCOVERY 10 1.5 RECENT LEUKEMIA MICROARRAY STUDIES 12 1.6 CLASS DISCOVERY – METHODOLOGIES 13 2 RESULTS AND DISCUSSION 21 2.1 CLASS DISCOVERY WITHIN THE TEL-AML1 SUBTYPE 21 2.2 CLASS DISCOVERY WITHIN THE HYPERDIPLOID>50 SUBTYPE 32 3 MATERIALS AND METHODS 41 3.1 PATIENTS 41 3.2 PREPROCESSING AND FILTERING 41 3.3 UNSUPERVISED ANALYSIS 42 3.4 SUPERVISED ANALYSIS 43 4 SUMMARY 46 REFRENCES 48 APPENDIX 53 Abstract Leukemia is not a single homogenous disease and can be divided into subtypes, based on the associated chromosomal abnormalities. Recently, using microarray data analysis, several research groups characterized the gene expression profiles of different, previously known, leukemia subtypes. Our aim was class discovery: to identify new partitions of leukemia samples, into novel sub-groups with no previously known common label, on the basis of their gene expression profiles.
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