CPA4 Antibody Cat

Total Page：16

File Type：pdf, Size：1020Kb

CPA4 Antibody Cat. No.: 62-835 CPA4 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This CPA4 antibody is generated from rabbits immunized with a KLH conjugated synthetic IMMUNOGEN: peptide between 305-336 amino acids from the C-terminal region of human CPA4. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 47 kDa WEIGHT: Properties This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by PURIFICATION: dialysis CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid October 1, 2021 1 https://www.prosci-inc.com/cpa4-antibody-62-835.html BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: CPA4 ALTERNATE NAMES: Carboxypeptidase A4, 3417-, Carboxypeptidase A3, CPA4, CPA3 ACCESSION NO.: Q9UI42 PROTEIN GI NO.: 61252703 GENE ID: 51200 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References CPA4 is a member of the carboxypeptidase A/B subfamily. Carboxypeptidases are zinc- containing exopeptidases that catalyze the release of carboxy-terminal amino acids, and BACKGROUND: are synthesized as zymogens that are activated by proteolytic cleavage. This protein could be involved in the histone hyperacetylation pathway. It is imprinted and may be a strong candidate protein for prostate cancer aggressiveness. REFERENCES: 1) Ross,P.L., Cheng,I. BMC Cancer 9, 69 (2009) 2) Bentley,L., Nakabayashi,K. J. Med. Genet. 40 (4), 249-256 (2003) 3) Kayashima,T., Yamasaki,K. Hum. Genet. 112 (3), 220-226 (2003) 4) Hayashida,S., Yamasaki,K. Genomics 66 (2), 221-225 (2000) ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. October 1, 2021 2 https://www.prosci-inc.com/cpa4-antibody-62-835.html.

Copy Link

Recommended publications

Detailed Characterization of Human Induced Pluripotent Stem Cells Manufactured for Therapeutic Applications
Stem Cell Rev and Rep DOI 10.1007/s12015-016-9662-8 Detailed Characterization of Human Induced Pluripotent Stem Cells Manufactured for Therapeutic Applications Behnam Ahmadian Baghbaderani 1 & Adhikarla Syama2 & Renuka Sivapatham3 & Ying Pei4 & Odity Mukherjee2 & Thomas Fellner1 & Xianmin Zeng3,4 & Mahendra S. Rao5,6 # The Author(s) 2016. This article is published with open access at Springerlink.com Abstract We have recently described manufacturing of hu- help determine which set of tests will be most useful in mon- man induced pluripotent stem cells (iPSC) master cell banks itoring the cells and establishing criteria for discarding a line. (MCB) generated by a clinically compliant process using cord blood as a starting material (Baghbaderani et al. in Stem Cell Keywords Induced pluripotent stem cells . Embryonic stem Reports, 5(4), 647–659, 2015). In this manuscript, we de- cells . Manufacturing . cGMP . Consent . Markers scribe the detailed characterization of the two iPSC clones generated using this process, including whole genome se- quencing (WGS), microarray, and comparative genomic hy- Introduction bridization (aCGH) single nucleotide polymorphism (SNP) analysis. We compare their profiles with a proposed calibra- Induced pluripotent stem cells (iPSCs) are akin to embryonic tion material and with a reporter subclone and lines made by a stem cells (ESC) [2] in their developmental potential, but dif- similar process from different donors. We believe that iPSCs fer from ESC in the starting cell used and the requirement of a are likely to be used to make multiple clinical products. We set of proteins to induce pluripotency [3]. Although function- further believe that the lines used as input material will be used ally identical, iPSCs may differ from ESC in subtle ways, at different sites and, given their immortal status, will be used including in their epigenetic profile, exposure to the environ- for many years or even decades.
[Show full text]
Mouse Cpa4 Knockout Project (CRISPR/Cas9)
http://www.alphaknockout.com/ Mouse Cpa4 Knockout Project (CRISPR/Cas9) Objective: To create a Cpa4 knockout mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Cpa4 gene ( NCBI Reference Sequence: NM_027926 ; Ensembl: ENSMUSG00000039070 ) is located on mouse chromosome 6. 11 exons are identified , with the ATG start codon in exon 1 and the TAG stop codon in exon 11 (Transcript: ENSMUST00000049251). Exon 2~10 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 starts from about 5.48% of the coding region. Exon 2~10 covers 79.92% of the coding region. The size of effective KO region: ~12130 bp. Page 1 of 8 http://www.alphaknockout.com/ Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 3 4 5 6 7 8 9 10 11 Legends Exon of mouse Cpa4 Knockout region Page 2 of 8 http://www.alphaknockout.com/ Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section upstream of Exon 2 is aligned with itself to determine if there are tandem repeats. No significant tandem repeat is found in the dot plot matrix. So this region is suitable for PCR screening or sequencing analysis. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section downstream of Exon 10 is aligned with itself to determine if there are tandem repeats.
[Show full text]
Language Impairment Resulting from a De Novo Deletion of 7Q32.1-Q33: a Case
bioRxiv preprint doi: https://doi.org/10.1101/047241; this version posted April 6, 2016. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Language impairment resulting from a de novo deletion of 7q32.1-q33: a case report Mª Salud Jiménez-Romero, Montserrat Barcos-Martínez, Isabel Espejo-Portero, Antonio Benítez-Burraco Corresponding author: Antonio Benítez-Burraco, PhD. Department of Spanish Philology and its Didactics, University of Huelva, Huelva, Spain e-mail: [email protected] Affiliations for the other authors: Mª Salud Jiménez-Romero: Department of Psychology, University of Córdoba, Córdoba, Spain & Maimónides Institute of Biomedical Research, Córdoba, Spain Montserrat Barcos-Martínez: Laboratory of Molecular Genetics, University Hospital “Reina Sofía”, Córdoba, Spain &Maimónides Institute of Biomedical Research, Córdoba, Spain Isabel Espejo-Portero: Laboratory of Molecular Genetics, University Hospital “Reina Sofía”, Córdoba, Spain & Maimónides Institute of Biomedical Research, Córdoba, Spain bioRxiv preprint doi: https://doi.org/10.1101/047241; this version posted April 6, 2016. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 2 ABSTRACT Chromosome 7 is a hot spot for cognitive disorders involving language deficits. We report on a girl who presents with a cognitive and speech delay, motor problems, hearing loss, and behavioral disturbances, and a de novo deletion within 7q32.1-q33 (chromosome position: chr7:127109685-132492196, hg 18). Several genes involved in brain development and function are located within the deleted region.
[Show full text]
Aïda Homs Raubert
Epigenetic alterations in autism spectrum disorders (ASD) Aïda Homs Raubert DOCTORAL THESIS UPF 2015 THESIS SUPERVISORS Prof. Luis A. Pérez Jurado Dra. Ivon Cuscó Martí DEPARTAMENT DE CIÈNCIES EXPERIMENTALS I DE LA SALUT Als meus pares, a l’Alexandra a l’Agustí i als bessons que vindran iii ACKNOWLEDGEMENTS Aquesta no és nomes la meva tesi, en ella han contribuït moltes persones, tant de l’entorn del parc de recerca, de terres lleidatanes, Berguedanes i fins i tot de l’altra banda de l’Atlàntic. Primer, volia agrair als directors de tesi, al Prof. Luis Pérez Jurado i a la Dra. Ivon Cuscó, tot el temps dedicat a revisar i corregir els raonaments i les paraules en aquesta tesi, ja que sempre han tingut la porta oberta per atendre qualsevol dubte. També per haver-me ensenyat una metodologia, un rigor i un llenguatge científic, on l’entrenament és necessari per assolir els conceptes per la recerca en concret, i pel món de la ciència i la genètica. Gràcies per la dedicació, la paciencia, la feina i energia dipositada. No hagués arribat al mateix port si al laboratori no m’hagués trobat amb persones que m’inspiren. Primer de tot, a les nenes: a la Gabi, la companya de vaixell fins i tot el dia de dipositar la tesi, perquè sobretot ens hem sabut acompanyar i entendre malgrat tenir altres maneres de funcionar, gràcies. També a la Marta i la Cristina, que amb la seva honestedat i bona fe, omplen el laboratori de bones energies, gràcies per ser-hi en tot moment.
[Show full text]
Identification of SCARA3 with Potential Roles in Metabolic Disorders
www.aging-us.com AGING 2021, Vol. 13, No. 2 Research Paper Identification of SCARA3 with potential roles in metabolic disorders Hui Peng1, Qi Guo1, Tian Su1, Ye Xiao1, Chang-Jun Li1, Yan Huang1, Xiang-Hang Luo1 1Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, China Correspondence to: Yan Huang, Xiang-Hang Luo; email: [email protected], [email protected] Keywords: adipogenesis, obesity, SCARA3, methylation, metabolic disorders Received: July 22, 2020 Accepted: October 22, 2020 Published: December 9, 2020 Copyright: © 2020 Peng 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 Obesity is characterized by the expansion of adipose tissue which is partially modulated by adipogenesis. In the present study, we identified five differentially expressed genes by incorporating two adipogenesis-related datasets from the GEO database and their correlation with adipogenic markers. However, the role of scavenger receptor class A member 3 (SCARA3) in obesity-related disorders has been rarely reported. We found that Scara3 expression in old adipose tissue-derived mesenchymal stem cells (Ad-MSCs) was lower than it in young Ad-MSCs. Obese mice caused by deletion of the leptin receptor gene (db/db) or by a high-fat diet both showed reduced Scara3 expression in inguinal white adipose tissue. Moreover, hypermethylation of SCARA3 was observed in patients with type 2 diabetes and atherosclerosis. Data from the CTD database indicated that SCARA3 is a potential target for metabolic diseases.
[Show full text]
Mouse Cpa4 Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Cpa4 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Cpa4 conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Cpa4 gene (NCBI Reference Sequence: NM_027926 ; Ensembl: ENSMUSG00000039070 ) is located on Mouse chromosome 6. 11 exons are identified, with the ATG start codon in exon 1 and the TAG stop codon in exon 11 (Transcript: ENSMUST00000049251). Exon 2~3 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Cpa4 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-368N11 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 starts from about 5.48% of the coding region. The knockout of Exon 2~3 will result in frameshift of the gene. The size of intron 1 for 5'-loxP site insertion: 5401 bp, and the size of intron 3 for 3'-loxP site insertion: 1549 bp. The size of effective cKO region: ~1136 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 3 4 11 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Cpa4 Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats.
[Show full text]
The Imprinted Region on Human Chromosome 7Q32 Extends to The
249 ORIGINAL ARTICLE J Med Genet: first published as 10.1136/jmg.40.4.249 on 1 April 2003. Downloaded from The imprinted region on human chromosome 7q32 extends to the carboxypeptidase A gene cluster: an imprinted candidate for Silver-Russell syndrome L Bentley, K Nakabayashi, D Monk, C Beechey, J Peters, Z Birjandi, F E Khayat, M Patel, M A Preece, P Stanier, S W Scherer, G E Moore ............................................................................................................................. J Med Genet 2003;40:249–256 See end of article for authors’ affiliations Imprinted gene(s) on human chromosome 7q32-qter have been postulated to be involved in intrauterine ....................... growth restriction associated with Silver-Russell syndrome (SRS) as 7-10% of patients have mUPD(7). Correspondence to: Three imprinted genes, MEST, MESTIT1, and COPG2IT1 on chromosome 7q32, are unlikely to cause L Bentley, Department of SRS since epigenetic and sequence mutation analyses have not shown any changes. One hundred Fetal and Maternal kilobases proximal to MEST lies a group of four carboxypeptidase A (CPA) genes. Since most imprinted Medicine, Institute of genes are found in clusters, this study focuses on analysing these CPAs for imprinting effects based on Reproductive and Developmental Biology, their proximity to an established imprinted domain. Firstly, a replication timing study across 7q32 Faculty of Medicine, showed that an extensive genomic region including the CPAs, MEST, MESTIT1, and COPG2IT1 repli- Imperial College, cates asynchronously. Subsequently, SNP analysis by sequencing RT-PCR products of CPA1, CPA2, Hammersmith Campus, CPA4, and CPA5 indicated preferential expression of CPA4. Pyrosequencing was used as a quantita- Du Cane Road, London tive approach, which confirmed predominantly preferential expression of the maternal allele and bial- W12 0NN, UK; [email protected] lelic expression in brain.
[Show full text]
Epigenetic Silencing of Novel Tumor Suppressors in Malignant Melanoma
Research Article Epigenetic Silencing of Novel Tumor Suppressors in Malignant Melanoma Viswanathan Muthusamy,1 Sekhar Duraisamy,2 C. Matthew Bradbury,1 Cara Hobbs,1 David P. Curley,1 Betsy Nelson,1 and Marcus Bosenberg1 1Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont and 2Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts Abstract infrequent in the genome but are associated with the promoter regions of nearly half of all known human genes (10). Examination Malignant melanoma is a common and frequently lethal disease. Current therapeutic interventions have little effect on of familial cancer genes has revealed that tumor-specific hyper- survival, emphasizing the need for a better understanding of methylation may act as a second hit by preferentially targeting the genetic, epigenetic, and phenotypic changes in melanoma the wild-type allele of tumor suppressors, whereas the promoter region of the mutant allele is not affected by methylation (11). formation and progression. We identified 17 genes that were de novo Dnmt1 not previously known to be silenced by methylation in Inhibition of methylation by down-regulation has melanoma using a microarray-based screen following treat- been shown to reduce tumor formation in several settings (12–14). Decreased Dnmt1 function completely suppressed polyp formation ment of melanoma cell lines with the DNA methylation ApcMin/+ inhibitor 5-Aza-2¶-deoxycytidine. Eight of these genes have in mice, showing that aberrant hypermethylation events not been previously shown to undergo DNA methylation in any are necessary to form and maintain tumors (12, 13, 15). However, in QPCT, CYP1B1 LXN other cases, genomic hypomethylation induced by down-regulation form of cancer.
[Show full text]
In the Human Genome
bioRxiv preprint doi: https://doi.org/10.1101/239053; this version posted December 23, 2017. 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. Alignment-Free Approaches Predict Novel Nuclear Mitochondrial Segments (NUMTs) in the Human Genome Wentian Li, Jerome Freudenberg The Robert S. Boas Center for Genomics and Human Genetics The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, USA December 2017 Abstract Regions of the nuclear genome may harbor sequences of mitochondrial origin, indicating an ancestral trans- fer of mitochondrial DNA into the nuclear genome. These Nuclear Mitochondrial Segments (NUMTs) are traditionally detected by sequence similarity search, as implemented in the Basic Local Alignment Search Tool (BLAST). Conﬁdently detecting such NUMTs is important for the comprehensive annotation of the human genome. Here we explore the possibility of detecting NUMTs in the human genome by alignment-free ap- proaches, such as k-mers (k-tuples, k-grams, oligos of length k) distributions. We ﬁnd that when k=6 or larger, the k-mer approach and BLAST search produce almost identical results, e.g., detect the same set of NUMTs longer than 3kb. However, when k=5 or k=4, certain signals are only detected by the alignment-free approach, and these may indicate yet unrecognized, and potentially more ancestral NUMTs. We introduce a “Manhattan plot” style representation of NUMTs predictions across the genome, which are calculated based on the reciprocal of the Jensen-Shannon divergence between the nuclear and mitochondrial k-mer frequencies.
[Show full text]
A Noncanonical Mechanism of Carboxypeptidase Inhibition Revealed by the Crystal Structure of the Tri-Kunitz Smci in Complex with Human CPA4
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Structure Article A Noncanonical Mechanism of Carboxypeptidase Inhibition Revealed by the Crystal Structure of the Tri-Kunitz SmCI in Complex with Human CPA4 Maday Alonso del Rivero,3,4 Mey L. Reytor,3,4 Sebastian A. Trejo,1,2 Marıá A. Cha´ vez,3 Francesc X. Avile´ s,1,* and David Reverter1,* 1Institut de Biotecnologia i de Biomedicina and Departament de Bioquı´mica i de Biologia Molecular 2Servei de Proteomica i Biologia Estructural (SePBioEs-UAB) Universitat Auto` noma de Barcelona, 08193 Bellaterra, Barcelona, Spain 3Centro de Estudio de Proteıńas, Facultad de Biologıá, Universidad de la Habana, Cuba 10400 4These authors contributed equally to this work *Correspondence: [email protected] (F.X.A.), [email protected] (D.R.) http://dx.doi.org/10.1016/j.str.2013.04.021 SUMMARY ples of natural protein inhibitors have been reported, only a few of them are known for MCPs. Protein inhibitors of MCPs have The crystal structure of SmCI (Sabellastarte magnifica been identified and characterized from the following sources: carboxypeptidase inhibitor) has been determined in in Solanacea, i.e., tomato and potato (PCI) (Arolas et al., 2007; complex with human carboxypeptidase A4 (hCPA4). Rees and Lipscomb, 1982); in the intestinal parasite Ascaris SmCI is composed by three BPTI/Kunitz domains, suum (ACI) (Sanglas et al., 2009); in the medicinal leech Hirudo each one displaying high structural homology and medicinalis (LCI) (Reverter et al., 2000); in the ticks Rhipicephalus functionality with serine protease inhibitors.
[Show full text]
Insights Into the Specificity and Function of M14 Metallocarboxypeptidases From
Insights into the specificity and function of M14 metallocarboxypeptidases from structural and degradomic studies Sebastian Martin Tanco Insights into the specificity and function of M14 metallocarboxypeptidases from structural and degradomic studies Doctoral thesis presented by Sebastian Martin Tanco for the degree of PhD in Structure and Function of Proteins from the Universitat Autònoma de Barcelona Institut de Biotecnologia i Biomedicina Unitat d’Enginyeria de Proteïnes i Proteòmica Thesis supervised by Prof. Julia Lorenzo Rivera and Prof. Francesc Xavier Avilés Puigvert Sebastian Martin Tanco Prof. Julia Lorenzo Rivera Prof. Francesc Xavier Avilés Puigvert Barcelona, September 2012 A mi familia, y a todos aquellos que en estos años actuaron como si lo fueran Table of Contents Table of contents TABLE OF CONTENTS 9 ABBREVIATIONS 15 PREFACE 21 NOTE ABOUT THE FORMAT 23 BACKGROUND B.1. Proteases 27 B.2. Classification of proteases 29 B.3. Specificity-subsite terminology 32 B.4. Carboxypeptidases 33 B.5. Metallocarboxypeptidases 35 B.6. M14A metallocarboxypeptidases 36 B.7. M14B metallocarboxypeptidases 38 B.8. Cytosolic metallocarboxypeptidases 40 B.9. Structure of metallocarboxypeptidases 42 OBJECTIVES 47 CHAPTER 1 - Structure-function analysis of the short splicing-variant carboxypeptidase encoded by Drosophila melanogaster silver. 1.1. Introduction 51 1.2. Experimental section 56 1.3. Results and discussion 62 9 Table of contents CHAPTER 2 - Human carboxypeptidase A4: Characterization of the substrate specificity and implications for a role in extracellular peptide processing 2.1. Introduction 79 2.2. Experimental section 82 2.3. Results 88 2.4. Discussion 106 CHAPTER 3 - Proteome-derived peptide libraries to study the substrate specificity profiles of carboxypeptidases.
[Show full text]
CPA4 (NM 016352) Human Tagged ORF Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC208575L4 CPA4 (NM_016352) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: CPA4 (NM_016352) Human Tagged ORF Clone Tag: mGFP Symbol: CPA4 Synonyms: CPA3 Vector: pLenti-C-mGFP-P2A-Puro (PS100093) E. coli Selection: Chloramphenicol (34 ug/mL) Cell Selection: Puromycin ORF Nucleotide The ORF insert of this clone is exactly the same as(RC208575). Sequence: Restriction Sites: SgfI-MluI Cloning Scheme: ACCN: NM_016352 ORF Size: 1263 bp This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 CPA4 (NM_016352) Human Tagged ORF Clone – RC208575L4 OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_016352.2 RefSeq Size: 2817 bp RefSeq ORF: 1266 bp Locus ID: 51200 UniProt ID: Q9UI42, A4D1M3 Domains: Zn_carbOpept, Propep_M14 Protein Families: Druggable Genome, Protease, Secreted Protein MW: 47.4 kDa Gene Summary: This gene is a member of the carboxypeptidase A/B subfamily, and it is located in a cluster with three other family members on chromosome 7.
[Show full text]