HER3/Erbb3 (Phospho-Tyr1222) Antibody

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Product Datasheet HER3/ErbB3 (Phospho-Tyr1222) Antibody Catalog No: #13116 Package Size: #13116-1 50ul #13116-2 100ul Orders: [email protected] Support: [email protected] Description Product Name HER3/ErbB3 (Phospho-Tyr1222) Antibody Host Species Rabbit Clonality Polyclonal Purification The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho- and non-phospho-peptide affinity columns. Applications WB Species Reactivity Hu, Ms, Rt Specificity Phospho-HER3/ErbB3 (Phospho-Tyr1222) Antibody detects endogenous levels of HER3/ErbB3 only when phosphorylated at Tyr1222 Immunogen Type peptide Immunogen Description A synthesized peptide derived from human HER3/ErbB3 around the phosphorylation site of Tyr1222 Target Name HER3/ErbB3 Other Names c erbB 3; c erbB3; Erb b2 receptor tyrosine kinase 3; ErbB 3; ERBB3; ERBB3 protein; erbB3 S; ERBB3_HUMAN; Glial growth factor receptor; HER 3; HER3; Human epidermal growth factor receptor 3; LCCS2; MDA BF 1; MGC88033; p180 ErbB3; p45 sErbB3; p85 sErbB3; proto-oncogene-like protein c ErbB 3; proto-oncogene-like protein c ErbB3; Proto-oncogene-like protein c-ErbB-3; Receptor tyrosine protein kinase erbB 3; Receptor tyrosine protein kinase erbB3; Receptor tyrosine-protein kinase erbB-3; Tyrosine kinase type cell surface receptor HER3; Tyrosine kinase-type cell surface receptor HER3; v erb b2 avian erythroblastic leukemia viral oncogene homolog 3; v erb b2 erythroblastic leukemia viral oncogene homolog 3 (avian); v erb b2 erythroblastic leukemia viral oncogene homolog 3; Accession No. Swiss-Prot#:P21860NCBI Gene ID:2065 Calculated MW 148 Concentration 1mg/ml Formulation Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Storage Store at -20 °C.Stable for 12 months from date of receipt Application Details WB: 1:500-1:2000 Images Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 1 Western blot analysis of Phospho-HER3/ErbB3 (Tyr1222) in lysates of HuvEc EGF 200ng/ml 30', using Phospho-HER3/ErbB3 (Tyr1222) Antibody(13116). Note: This product is for in vitro research use only and is not intended for use in humans or animals. Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 2.

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Ret Oncogene and Thyroid Carcinoma
ndrom Sy es tic & e G n e e n G e f T o Elisei et al., J Genet Syndr Gene Ther 2014, 5:1 Journal of Genetic Syndromes h l e a r n a DOI: 10.4172/2157-7412.1000214 r p u y o J & Gene Therapy ISSN: 2157-7412 Review Article Open Access Ret Oncogene and Thyroid Carcinoma Elisei R, Molinaro E, Agate L, Bottici V, Viola D, Biagini A, Matrone A, Tacito A, Ciampi R, Vivaldi A and Romei C* Endocrine Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy Abstract Thyroid cancer is a malignant neoplasm that originates from follicular or parafollicular thyroid cells and is categorized as papillary (PTC), follicular (FTC), anaplastic (ATC) or medullary thyroid carcinoma (MTC). The alteration of the Rearranged during trasfection (RET) (proto-oncogene, a gene coding for a tyrosine-kinase receptor involved in the control of cell differentiation and proliferation, has been found to cause PTC and MTC. In particular, RET/PTC rearrangements and RET point mutations are related to PTC and MTC, respectively. Although RET/PTC rearrangements have been identified in both spontaneous and radiation-induced PTC, they occur more frequently in radiation-associated tumors. RET/PTC rearrangements have also been reported in follicular adenomas. Although controversial, correlations between RET/PTC rearrangements, especially RET/PTC3, and a more aggressive phenotype and a more advanced stage have been identified. Germline point mutations in the RET proto-oncogene are associated with nearly all cases of hereditary MTC, and a strict correlation between genotype and phenotype has been demonstrated.
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A Gain-Of-Function P53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia Through the Pluripotency Factor FOXH1
Published OnlineFirst May 8, 2019; DOI: 10.1158/2159-8290.CD-18-1391 RESEARCH ARTICLE A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Evangelia Loizou1,2, Ana Banito1, Geulah Livshits1, Yu-Jui Ho1, Richard P. Koche3, Francisco J. Sánchez-Rivera1, Allison Mayle1, Chi-Chao Chen1, Savvas Kinalis4, Frederik O. Bagger4,5, Edward R. Kastenhuber1,6, Benjamin H. Durham7, and Scott W. Lowe1,8 Downloaded from cancerdiscovery.aacrjournals.org on September 27, 2021. © 2019 American Association for Cancer Research. Published OnlineFirst May 8, 2019; DOI: 10.1158/2159-8290.CD-18-1391 ABSTRACT Mutations in the TP53 tumor suppressor gene are common in many cancer types, including the acute myeloid leukemia (AML) subtype known as complex karyotype AML (CK-AML). Here, we identify a gain-of-function (GOF) Trp53 mutation that accelerates CK-AML initiation beyond p53 loss and, surprisingly, is required for disease maintenance. The Trp53 R172H muta- tion (TP53 R175H in humans) exhibits a neomorphic function by promoting aberrant self-renewal in leu- kemic cells, a phenotype that is present in hematopoietic stem and progenitor cells (HSPC) even prior to their transformation. We identify FOXH1 as a critical mediator of mutant p53 function that binds to and regulates stem cell–associated genes and transcriptional programs. Our results identify a context where mutant p53 acts as a bona fi de oncogene that contributes to the pathogenesis of CK-AML and suggests a common biological theme for TP53 GOF in cancer. SIGNIFICANCE: Our study demonstrates how a GOF p53 mutant can hijack an embryonic transcrip- tion factor to promote aberrant self-renewal.
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Wnt-Independent and Wnt-Dependent Effects of APC Loss on the Chemotherapeutic Response
International Journal of Molecular Sciences Review Wnt-Independent and Wnt-Dependent Eﬀects of APC Loss on the Chemotherapeutic Response Casey D. Stefanski 1,2 and Jenifer R. Prosperi 1,2,3,* 1 Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46617, USA; [email protected] 2 Mike and Josie Harper Cancer Research Institute, South Bend, IN 46617, USA 3 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine-South Bend, South Bend, IN 46617, USA * Correspondence: [email protected]; Tel.: +1-574-631-4002 Received: 30 September 2020; Accepted: 20 October 2020; Published: 22 October 2020 Abstract: Resistance to chemotherapy occurs through mechanisms within the epithelial tumor cells or through interactions with components of the tumor microenvironment (TME). Chemoresistance and the development of recurrent tumors are two of the leading factors of cancer-related deaths. The Adenomatous Polyposis Coli (APC) tumor suppressor is lost in many diﬀerent cancers, including colorectal, breast, and prostate cancer, and its loss correlates with a decreased overall survival in cancer patients. While APC is commonly known for its role as a negative regulator of the WNT pathway, APC has numerous binding partners and functional roles. Through APC’s interactions with DNA repair proteins, DNA replication proteins, tubulin, and other components, recent evidence has shown that APC regulates the chemotherapy response in cancer cells. In this review article, we provide an overview of some of the cellular processes in which APC participates and how they impact chemoresistance through both epithelial- and TME-derived mechanisms. Keywords: adenomatous polyposis coli; chemoresistance; WNT signaling 1.
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Targeting the Function of the HER2 Oncogene in Human Cancer Therapeutics
Oncogene (2007) 26, 6577–6592 & 2007 Nature Publishing Group All rights reserved 0950-9232/07 $30.00 www.nature.com/onc REVIEW Targeting the function of the HER2 oncogene in human cancer therapeutics MM Moasser Department of Medicine, Comprehensive Cancer Center, University of California, San Francisco, CA, USA The year 2007 marks exactly two decades since human HER3 (erbB3) and HER4 (erbB4). The importance of epidermal growth factor receptor-2 (HER2) was func- HER2 in cancer was realized in the early 1980s when a tionally implicated in the pathogenesis of human breast mutationally activated form of its rodent homolog neu cancer (Slamon et al., 1987). This finding established the was identified in a search for oncogenes in a carcinogen- HER2 oncogene hypothesis for the development of some induced rat tumorigenesis model(Shih et al., 1981). Its human cancers. An abundance of experimental evidence human homologue, HER2 was simultaneously cloned compiled over the past two decades now solidly supports and found to be amplified in a breast cancer cell line the HER2 oncogene hypothesis. A direct consequence (King et al., 1985). The relevance of HER2 to human of this hypothesis was the promise that inhibitors of cancer was established when it was discovered that oncogenic HER2 would be highly effective treatments for approximately 25–30% of breast cancers have amplifi- HER2-driven cancers. This treatment hypothesis has led cation and overexpression of HER2 and these cancers to the development and widespread use of anti-HER2 have worse biologic behavior and prognosis (Slamon antibodies (trastuzumab) in clinical management resulting et al., 1989).
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Extensive Analysis of the Retinoblastoma Gene in Adult T Cell Leukemia/Lymphoma (ATL) Y Hatta1, Y Yamada2, M Tomonaga2 and HP Koeffler1
Leukemia (1997) 11, 984–989 1997 Stockton Press All rights reserved 0887-6924/97 $12.00 Extensive analysis of the retinoblastoma gene in adult T cell leukemia/lymphoma (ATL) Y Hatta1, Y Yamada2, M Tomonaga2 and HP Koeffler1 1Division of Hematology/Oncology, Department of Medicine, Cedars-Sinai Research Institute, UCLA School of Medicine, Los Angeles, CA, USA; and 2Department of Hematology, Atomic Disease Institute, Nagasaki University, School of Medicine, Nagasaki, Japan The retinoblastoma susceptibility gene (Rb) plays a key role in Tax;38 a long period of clinical latency (20–30 years) precedes regulating the cell cycle in association with cyclins and cyclin- the development of ATL;39,40 only a small percentage of dependent kinases (CDKs). Alteration of the Rb gene as well 40 as CDK inhibitors (CDKIs) leads to deregulated cellular growth HTLV-I-infected individuals develop this malignancy; and which promotes cancer formation. We examined the genomic ATL cells are monoclonal. configuration of the entire Rb gene in 40 primary adult T cell The missense inactivating mutations of the p53 gene have leukemias/lymphomas (ATL) and two ATL cell lines by South- been observed in ATL.41–44 We tested for the inactivation of ern blotting and also by polymerase chain reaction-single several CDK inhibitors (CDKIs) including p15INK4B, p16INK4A, strand conformation polymorphism (PCR-SSCP) analyses. p18INK4C, p19INK4D and p27KIP1, and have found deletions of Homozygous loss of exon 1 was identified in one of 21 acute the p16INK4A gene in 10 of 37 cases (27%); deletions of the ATL, one of 15 chronic ATL, and none of four lymphomatous INK4B 45 ATL samples.
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Physical Interaction of the Retinoblastoma Protein with Human D Cyclins
Cell, Vol. 73, 499-511, May 7, 1993, Copyright 0 1993 by Cell Press Physical Interaction of the Retinoblastoma Protein with Human D Cyclins Steven F. Dowdy,* Philip W. Hinds,’ Kenway Louie,’ into Rb- tumor cells by microinjection, viral infection, or Steven I. Reed,t Andrew Arnold,* transfection can lead to the growth arrest of these recipient and Robert A. Weinberg” cells (Huang et al., 1988; Goodrich et al., 1991; Templeton *The Whitehead Institute for Biomedical Research et al., 1991; Hinds et al., 1992). and Department of Biology Oncoproteins specified by the SV40, adenovirus, and Massachusetts Institute of Technology papilloma DNA tumor viruses have been shown to associ- Cambridge, Massachusetts 02142 ate with pRb in virus-transformed cells (Whyte et al., 1988; tThe Scripps Research Institute DeCaprio et al., 1988; Dyson et al., 1989). Oncoprotein Department of Molecular Biology binding of pRb is presumed to lead to its sequestration 10666 North Torrey Pines Road and functional inactivation. Conserved region II mutants La Jolla, California 92037 of adenovirus ElA, SV40 large T antigen, human papil- *Endocrine Unit loma E7 viral oncoproteins that have lost their ability to and Massachusetts General Hospital Cancer Center bind pflb, and other pRb-related proteins exhibit signifi- Massachusetts General Hospital cantly reduced transforming potential (Moran et al., 1986; and Harvard Medical School Lillie et al., 1987; Cherington et al., 1988; DeCaprio et al., Boston, Massachusetts 02114 1988; Moran, 1988; Smith and Ziff, 1988; Whyte et al., 1989). This suggests that binding of pRb and related pro- teins by these oncoproteins is critical to their transforming abilities.
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Updated November 2019 KIT Mutation the KIT Gene Is Associated With
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Genetic Testing for Germline Mutations of the RET Proto-Oncogene AHS - M2078
Corporate Medical Policy Genetic Testing for Germline Mutations of the RET Proto-Oncogene AHS - M2078 File Name: genetic_testing_for_germline_mutations_of_the_ret_proto-oncogene Origination: 1/2019 Last CAP Review 3/2021 Next CAP Review: 3/2022 Last Review: 3/2021 Description of Procedure or Service The RET (rearranged during transfection) proto-oncogene encodes a transmembrane receptor tyrosine kinase (Takahashi, Ritz, & Cooper, 1985) that regulates a complex network of signal transduction pathways during development, survival, proliferation, differentiation, and migration of the enteric nervous system progenitor cells (Hedayati, Zarif Yeganeh, Sheikholeslami, & Afsari, 2016). Disruption of RET signaling by mutation, gene rearrangement, overexpression or transcriptional up-regulation of the RET gene is implicated in several human cancers (Plaza-Menacho, Mologni, & McDonald, 2014), most commonly thyroid, but also chronic myelomonocytic leukemia, acute myeloid leukemia, and lung, breast, pancreatic, and colon cancers (Gordon et al., 2018). Mutation of the RET gene in a germline cell results in an autosomal dominant hereditary cancer syndrome, multiple endocrine neoplasia type 2 (MEN2) characterized by medullary thyroid carcinoma (MTC), pheochromocytoma (PHEO), and primary parathyroid hyperplasia (PPTH). (Figlioli, Landi, Romei, Elisei, & Gemignani, 2013). This policy covers genetic testing for germline variants in the RET gene. For information on testing of tumors for RET variants to guide chemotherapy. Related Policies M2109 Molecular Panel Testing of Cancers to Identify Targeted Therapy M2030 Testing for Targeted Therapy of Non-Small-Cell Lung Cancer M2108 Molecular Markers in Fine Needle Aspirates of the Thyroid. ***Note: This Medical Policy is complex and technical. For questions concerning the technical language and/or specific clinical indications for its use, please consult your physician.
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P53 Regulates the Transcription of Its &Delta
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The Adenomatous Polyposis Coli Tumour Suppressor Gene Regulates C-MYC Transcription in Colon Cancer Cells
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Cancer Biology Introduction Proto-Oncogenes Tumor
Introduction • Tissue homeostasis depends on the regulated cell division and self-elimination (programmed cell Cancer Biology death) of each of its constituent members except its stem cells • A tumor arises as a result of uncontrolled cell division and failure for self-elimination Chapter 18 • Alterations in three groups of genes are responsible Eric J. Hall., Amato Giaccia, for the deregulated control mechanisms that are the hallmarks of cancer cells: proto-oncogenes, tumor- Radiobiology for the Radiologist supressor genes, and DNA stability genes Proto-oncogenes Tumor-suppressor genes • Proto-oncogenes are components of signaling • Tumor-suppressor genes are also components of networks that act as positive growth the same signaling networks as proto-oncogenes, except that they act as negative growth regulators regulators in response to mitogens, cytokines, • They modulate proliferation and survival by and cell-to-cell contact antagonizing the biochemical functions of proto- • A gain-of-function mutation in only one copy oncogenes or responding to unchecked growth signals of a protooncogene results in a dominantly • In contrast to oncogenes, inactivation of both acting oncogene that often fails to respond to copies of tumor-suppressor genes is required for extracellular signals loss of function in most cases DNA stability genes Mechanisms of carcinogenesis • DNA stability genes form a class of genes • A single genetic alteration that leads to the involved in both monitoring and activation of an oncogene or loss of a tumor maintaining
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Defective Human Retinoblastoma Protein Identified by Lack of Interaction with the E1A Oncoprotein I
[CANCER RESEARCH 54, 1098-111~4. Fcbru:lrv 15. It~941 Defective Human Retinoblastoma Protein Identified by Lack of Interaction with the E1A Oncoprotein I Marco G. Paggi, z Fabio MarteUi, Maurizio Fanciulli, Armando Felsani, Salvatore Sciacchitano, Marco Varmi, Tiziana Bruno, Carmine M. Carapella, and Aristide Floridi Laboratori di Metabolismo Celhdare e Farmacocinetica [M. G. P., M. E, M. V, T. B., A. FI.]; Biologia Moh'cohu'e [F. M., A. Fe.], Centtv Ricerca Sperimentah', Istituto Regina Elena per lo Studio e la Cura dei Tumori, Via delle Messi d'Oro, 156, O0158 Rome; Istituto Tecnologie Biomediche, C. N. R., Via Morgagni 30/E, 00161 Rome [A. Fe.]; Dipartimento Medicina Sperimentale, Universith "La Sapienza, '" Viale Regina Elena, 361, 00161 Rome [S. S.]: and Divisione di Neurochirurgia, lstituto Regina Elena per lo Studio e la Cura dei Tumori, Viale Regina Elena, 291, 00161 Rome,/C. M. C.], Italy ABSTRACT The retinoblastoma gene product, pRb, is a nuclear phosphoprotein with DNA-binding property (21, 22). Normal pRb shows a certain Inactivating mutations of the retinoblastoma susceptibility gene (Rb) microheterogeneity in SDS-PAGE, due to different degrees of phos- are involved in the pathogenesis of hereditary and sporadic retinoblas- phorylation, so that the protein is usually found between 105 and 114 toma. Alterations in the Rb gene have also been found in several other human tumors occurring with epidemiological incidence higher than that kDa of apparent molecular mass. The phosphorylation status of pRb of retinoblastoma. Four human malignant glioma cell lines were examined oscillates between an unphosphorylated or an underphosphorylated for abnormalities in the retinoblastoma gene product (pRb), using a pro- form (fast-migrating), during the Go-G~ phases of the cell cycle, and cedure based on the interaction of pRb with an in vitro-translated adeno- a fully phosphorylated form (slow-migrating), when the cell reaches virus E1A oncoprotein.
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