NIPA2 Rabbit Pab Antibody

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NIPA2 rabbit pAb antibody Catalog No : Source: Concentration : Mol.Wt. (Da): A18398 Rabbit 1 mg/ml 39600 Applications WB Reactivity Human, Mouse Dilution WB 1：500-2000 Storage -20°C/1 year Specificity This antibody detects endogenous levels of NIPA2 at Human/Mouse Source / Purification The antibody was affinity-purified from rabbit serum by affinity- chromatography using specific immunogen. Immunogen Synthesized peptide derived from human NIPA2 Uniprot No Q8N8Q9 Alternative names Form Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. Clonality Polyclonal Isotype IgG Conjugation Background This gene encodes a possible magnesium transporter. This gene is located adjacent to the imprinted domain in the Prader-Willi syndrome deletion region of chromosome 15. Alternate splicing results in multiple transcript variants. Pseudogenes of this gene are found on chromosomes 3, 7 and 21.[provided by RefSeq, May 2010], Other NIPA2, NIPA2 Produtc Images： Application Key: WB-Western IP-Immunoprecipitation IHC-Immunohistochemistry ChIP-Chromatin Immunoprecipitation IF-Immunofluorescence F-Flow Cytometry E-P-ELISA-Peptide A AAB Biosciences Products www.aabsci.cn FOR RESEARCH USE ONLY. NOT FOR HUMAN OR DIAGNOSTIC USE. Species Cross-Reactivity Key: H-Human M-Mouse R-Rat Hm-Hamster Mk-Monkey Vir-Virus Mi-Mink C-Chicken Dm-D. melanogaster X-Xenopus Z-Zebrafish B-Bovine Dg-Dog Pg-Pig Sc-S. cerevisiae Ce-C. elegans Hr-Horse All-All Species Expected Trademarks All product names and trademarks are the property of their respective owners. Regulatory Disclaimer For life science research only. Not for use in diagnostic procedures. Contact and Support: To ask questions, solve problems, suggest enhancements and report new applications, please visit our Online Technical Support Site. To call, write, fax, or email us, please visit www.aabsci.c n , contact information will be displayed. A AAB Biosciences Products www.aabsci.cn FOR RESEARCH USE ONLY. NOT FOR HUMAN OR DIAGNOSTIC USE..

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Variable Penetrance of the 15Q11.2 BP1–BP2 Microduplication in a Family With
bioRxiv preprint doi: https://doi.org/10.1101/095919; this version posted December 22, 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 The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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 Variable penetrance of the 15q11.2 BP1–BP2 microduplication in a family with cognitive and language impairment Antonio Benítez-Burraco1, Montserrat Barcos-Martínez 2,3, Isabel Espejo-Portero2,3, Mª Salud Jiménez-Romero2,4 1. Department of Philology, University of Huelva, Huelva, Spain 2. Maimónides Institute of Biomedical Research, Córdoba, Spain 3. Laboratory of Molecular Genetics, University Hospital “Reina Sofía”, Córdoba, Spain 4. Department of Psychology, University of Córdoba, Córdoba, Spain Corresponding author: Antonio Benítez-Burraco Área de Lengua Española. Departamento de Filología. Facultad de Humanidades. Campus de "El Carmen". Universidad de Huelva. Avda. de las Fuerzas Armadas s/n. 21071-Huelva (España) e-mail: [email protected] Contact details for the other authors: Mª Salud Jiménez-Romero: [email protected] Montserrat Barcos-Martínez: [email protected] Isabel Espejo-Portero: [email protected] bioRxiv preprint doi: https://doi.org/10.1101/095919; this version posted December 22, 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 The 15q11.2 BP1–BP2 region is found duplicated or deleted in people with cognitive, language, and behavioral impairment. Case presentation. We report on a family (the father and three male twin siblings) who presents with a duplication of the 15q11.2 BP1-BP2 region and a variable phenotype: whereas the father and the fraternal twin are normal carriers, the monozygotic twins exhibit severe language and cognitive delay and behavioral disturbances.
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Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders
177 Arch Neuropsychitry 2020;57:177−191 RESEARCH ARTICLE https://doi.org/10.29399/npa.24890 Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders Hakan GÜRKAN1 , Emine İkbal ATLI1 , Engin ATLI1 , Leyla BOZATLI2 , Mengühan ARAZ ALTAY2 , Sinem YALÇINTEPE1 , Yasemin ÖZEN1 , Damla EKER1 , Çisem AKURUT1 , Selma DEMİR1 , Işık GÖRKER2 1Faculty of Medicine, Department of Medical Genetics, Edirne, Trakya University, Edirne, Turkey 2Faculty of Medicine, Department of Child and Adolescent Psychiatry, Trakya University, Edirne, Turkey ABSTRACT Introduction: Aneuploids, copy number variations (CNVs), and single in 39 (39/123=31.7%) patients. Twelve CNV variant of unknown nucleotide variants in specific genes are the main genetic causes of significance (VUS) (9.75%) patients and 7 CNV benign (5.69%) patients developmental delay (DD) and intellectual disability disorder (IDD). were reported. In 6 patients, one or more pathogenic CNVs were These genetic changes can be detected using chromosome analysis, determined. Therefore, the diagnostic efficiency of CMA was found to chromosomal microarray (CMA), and next-generation DNA sequencing be 31.7% (39/123). techniques. Therefore; In this study, we aimed to investigate the Conclusion: Today, genetic analysis is still not part of the routine in the importance of CMA in determining the genomic etiology of unexplained evaluation of IDD patients who present to psychiatry clinics. A genetic DD and IDD in 123 patients. diagnosis from CMA can eliminate genetic question marks and thus Method: For 123 patients, chromosome analysis, DNA fragment analysis alter the clinical management of patients. Approximately one-third and microarray were performed. Conventional G-band karyotype of the positive CMA findings are clinically intervenable.
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In Silico Cancer Cell Versus Stroma Cellularity
Yang et al. BMC Medical Genomics 2014, 7(Suppl 1):S2 http://www.biomedcentral.com/1755-8794/7/S1/S2 RESEARCH Open Access In Silico cancer cell versus stroma cellularity index computed from species-specific human and mouse transcriptome of xenograft models: towards accurate stroma targeting therapy assessment Xinan Yang1,6, Yong Huang1, Younghee Lee1, Vincent Gardeux2,3,4,11, Ikbel Achour2,4,11, Kelly Regan2,4, Ellen Rebman2,4, Haiquan Li2,4,11, Yves A Lussier1,2,4,5,7,8,9,10,11* From The 3rd Annual Translational Bioinformatics Conference (TBC/ISCB-Asia 2013) Seoul, Korea. 2-4 October 2013 Abstract Background: The current state of the art for measuring stromal response to targeted therapy requires burdensome and rate limiting quantitative histology. Transcriptome measures are increasingly affordable and provide an opportunity for developing a stromal versus cancer ratio in xenograft models. In these models, human cancer cells are transplanted into mouse host tissues (stroma) and together coevolve into a tumour microenvironment. However, profiling the mouse or human component separately remains problematic. Indeed, laser capture microdissection is labour intensive. Moreover, gene expression using commercial microarrays introduces significant and underreported cross-species hybridization errors that are commonly overlooked by biologists. Method: We developed a customized dual-species array, H&M array, and performed cross-species and species- specific hybridization measurements. We validated a new methodology for establishing the stroma vs cancer ratio using transcriptomic data. Results: In the biological validation of the H&M array, cross-species hybridization of human and mouse probes was significantly reduced (4.5 and 9.4 fold reduction, respectively; p < 2x10-16 for both, Mann-Whitney test).
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Rabbit Anti-NIPA-2 Antibody-SL7465R
SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-NIPA-2 antibody SL7465R Product Name: NIPA-2 Chinese Name: 镁TransporterNIPA2抗体 Magnesium transporter NIPA2; MGC5466; NIPA 2; NIPA2_HUMAN; NIPA2; Non Alias: imprinted in Prader Willi/Angelman syndrome 2; Non imprinted in Prader Willi/Angelman syndrome region protein 2. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Chicken,Dog,Cow,Rabbit, WB=1:500-2000ELISA=1:500-1000IHC-P=1:400-800IHC-F=1:400-800ICC=1:100- 500IF=1:100-500（Paraffin sections need antigen repair） Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 36kDa Cellular localization: The cell membrane Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLHwww.sunlongbiotech.com conjugated synthetic peptide derived from human NIPA-2:251-360/360 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. PubMed: PubMed This gene encodes a possible magnesium transporter. This gene is located adjacent to the imprinted domain in the Prader-Willi syndrome deletion region of chromosome 15.
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BMC Genomics Biomed Central
BMC Genomics BioMed Central Research article Open Access Genomic analysis of the chromosome 15q11-q13 Prader-Willi syndrome region and characterization of transcripts for GOLGA8E and WHCD1L1 from the proximal breakpoint region Yong-hui Jiang*1, Kekio Wauki1,3, Qian Liu1, Jan Bressler1, Yanzhen Pan1, Catherine D Kashork1,2, Lisa G Shaffer1,2 and Arthur L Beaudet1 Address: 1Departments of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA, 2Signature Genomics Laboratories, LLC, 120 North Pine Street, Suite 242C, Spokane, WA 99202, USA and 3Shinshu University School of Medicine, Dept of Medical Genetics, 3-1-1 Asahi, Nagano, Matsumoto 390-8621, Japan Email: Yong-hui Jiang* - [email protected]; Kekio Wauki - [email protected]; Qian Liu - [email protected]; Jan Bressler - [email protected]; Yanzhen Pan - [email protected]; Catherine D Kashork - [email protected]; Lisa G Shaffer - [email protected]; Arthur L Beaudet - [email protected] * Corresponding author Published: 28 January 2008 Received: 20 September 2007 Accepted: 28 January 2008 BMC Genomics 2008, 9:50 doi:10.1186/1471-2164-9-50 This article is available from: http://www.biomedcentral.com/1471-2164/9/50 © 2008 Jiang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Prader-Willi syndrome (PWS) is a neurobehavioral disorder characterized by neonatal hypotonia, childhood obesity, dysmorphic features, hypogonadism, mental retardation, and behavioral problems.
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Magnesium Supplement and the 15Q11.2 BP1–BP2 Microdeletion (Burnside–Butler) Syndrome: a Potential Treatment?
International Journal of Molecular Sciences Commentary Magnesium Supplement and the 15q11.2 BP1–BP2 Microdeletion (Burnside–Butler) Syndrome: A Potential Treatment? Merlin G. Butler Departments of Psychiatry & Behavioral Sciences and Pediatrics, University of Kansas Medical Center, Kansas City, KS 66160, USA; [email protected]; Tel.: +1-913-588-1800 Received: 7 May 2019; Accepted: 12 June 2019; Published: 14 June 2019 Abstract: The 15q11.2 BP1–BP2 microdeletion (Burnside–Butler) syndrome is an emerging disorder that encompasses four genes (NIPA1, NIPA2, CYFIP1, and TUBGCP5). When disturbed, these four genes can lead to cognitive impairment, language and/or motor delay, psychiatric/behavioral problems (attention-deﬁcit hyperactivity, autism, dyslexia, schizophrenia/paranoid psychosis), ataxia, seizures, poor coordination, congenital anomalies, and abnormal brain imaging. This microdeletion was reported as the most common cytogenetic ﬁnding when using ultra-high- resolution chromosomal microarrays in patients presenting for genetic services due to autism with or without additional clinical features. Additionally, those individuals with Prader–Willi or Angelman syndromes having the larger typical 15q11–q13 type I deletion which includes the 15q11.2 BP1–BP2 region containing the four genes, show higher clinical severity than those having the smaller 15q11–q13 deletion where these four genes are intact. Two of the four genes (i.e., NIPA1 and NIPA2) are expressed in the brain and encode magnesium transporters. Magnesium is required in over 300 enzyme systems that are critical for multiple cellular functions, energy expenditure, protein synthesis, DNA transcription, and muscle and nerve function. Low levels of magnesium are found in those with seizures, depression, and acute or chronic brain diseases.
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Content Based Search in Gene Expression Databases and a Meta-Analysis of Host Responses to Infection
Content Based Search in Gene Expression Databases and a Meta-analysis of Host Responses to Infection A Thesis Submitted to the Faculty of Drexel University by Francis X. Bell in partial fulﬁllment of the requirements for the degree of Doctor of Philosophy November 2015 c Copyright 2015 Francis X. Bell. All Rights Reserved. ii Acknowledgments I would like to acknowledge and thank my advisor, Dr. Ahmet Sacan. Without his advice, support, and patience I would not have been able to accomplish all that I have. I would also like to thank my committee members and the Biomed Faculty that have guided me. I would like to give a special thanks for the members of the bioinformatics lab, in particular the members of the Sacan lab: Rehman Qureshi, Daisy Heng Yang, April Chunyu Zhao, and Yiqian Zhou. Thank you for creating a pleasant and friendly environment in the lab. I give the members of my family my sincerest gratitude for all that they have done for me. I cannot begin to repay my parents for their sacriﬁces. I am eternally grateful for everything they have done. The support of my sisters and their encouragement gave me the strength to persevere to the end. iii Table of Contents LIST OF TABLES.......................................................................... vii LIST OF FIGURES ........................................................................ xiv ABSTRACT ................................................................................ xvii 1. A BRIEF INTRODUCTION TO GENE EXPRESSION............................. 1 1.1 Central Dogma of Molecular Biology........................................... 1 1.1.1 Basic Transfers .......................................................... 1 1.1.2 Uncommon Transfers ................................................... 3 1.2 Gene Expression ................................................................. 4 1.2.1 Estimating Gene Expression ............................................ 4 1.2.2 DNA Microarrays ......................................................
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(Burnside-Butler) Syndrome in Five Families
International Journal of Molecular Sciences Article Genomic, Clinical, and Behavioral Characterization of 15q11.2 BP1-BP2 Deletion (Burnside-Butler) Syndrome in Five Families Isaac Baldwin 1,2,† , Robin L. Shafer 3,† , Waheeda A. Hossain 1,2, Sumedha Gunewardena 4, Olivia J. Veatch 1,4, Matthew W. Mosconi 3,5 and Merlin G. Butler 1,2,* 1 Department of Psychiatry & Behavioral Sciences, University of Kansas Medical Center, 3901 Rainbow Blvd. MS 4015, Kansas City, KS 66160, USA; [email protected] (I.B.); [email protected] (W.A.H.); [email protected] (O.J.V.) 2 Department of Pediatrics, University of Kansas Medical Center, 3901 Rainbow Blvd. MS 4015, Kansas City, KS 66160, USA 3 Schiefelbusch Institute for Life Span Studies and Kansas Center for Autism Research and Training, University of Kansas, Lawrence, KS 66045, USA; [email protected] (R.L.S.); [email protected] (M.W.M.) 4 Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA; [email protected] 5 Clinical Child Psychology Program, University of Kansas, Lawrence, KS 66045, USA * Correspondence: [email protected] † Represents co-first authorship. Abstract: The 15q11.2 BP1-BP2 deletion (Burnside-Butler) syndrome is emerging as the most com- mon cytogenetic finding in patients with neurodevelopmental or autism spectrum disorders (ASD) presenting for microarray genetic testing. Clinical findings in Burnside-Butler syndrome include developmental and motor delays, congenital abnormalities, learning and behavioral problems, and Citation: Baldwin, I.; Shafer, R.L.; abnormal brain findings. To better define symptom presentation, we performed comprehensive cog- Hossain, W.A.; Gunewardena, S.; Veatch, O.J.; Mosconi, M.W.; Butler, nitive and behavioral testing, collected medical and family histories, and conducted clinical genetic M.G.
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Microduplications at the 15Q11.2 BP1–BP2 Locus Are Enriched in Patients with Anorexia Nervosa T
Journal of Psychiatric Research 113 (2019) 34–38 Contents lists available at ScienceDirect Journal of Psychiatric Research journal homepage: www.elsevier.com/locate/jpsychires Microduplications at the 15q11.2 BP1–BP2 locus are enriched in patients with anorexia nervosa T Xiao Changa,1, Huiqi Qua,1, Yichuan Liua, Joseph Glessnera, Cuiping Houa, Fengxiang Wanga, ∗ Jin Lid, Patrick Sleimana,b,c, Hakon Hakonarsona,b,c, a The Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA b Department of Pediatrics, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA c Division of Human Genetics, Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA d Aﬃliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China ARTICLE INFO ABSTRACT Keywords: Microduplication at 15q11.2 have been reported in genetic association studies of schizophrenia and autism. Anorexia nervosa Given the potential overlap in psychiatric symptoms of schizophrenia and autism with anorexia nervosa (AN), Copy number variation we were inspired to test the association of this CNV locus with the genetic susceptibility of AN using ParseCNV, a CYFIP1 highly quality controlled CNV pipeline developed by our group. The CNV analysis was performed in 1017 AN NIPA1 cases and 7250 controls using the Illumina HumanHap610 SNP arrays data. We uncovered association of the NIPA2 15q11.2 microduplication with AN with P = 0.00023, while no genetic association between the microdeletion of this region and AN was identiﬁed. Among four genes in this region that are not imprinted, NIPA1 has the highest expression in brain and encodes a magnesium transporter protein on early endosomes and the cell surface in neurons.
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Methylation-Specific Multiplex Ligation-Dependent Probe
GENETIC TESTING AND MOLECULAR BIOMARKERS Volume 16, Number 3, 2012 ª Mary Ann Liebert, Inc. Pp. 178–186 DOI: 10.1089/gtmb.2011.0115 Methylation-Specific Multiplex Ligation-Dependent Probe Amplification and Identification of Deletion Genetic Subtypes in Prader-Willi Syndrome Rebecca S. Henkhaus,1 Soo-Jeong Kim,2 Virginia E. Kimonis,3 June-Anne Gold,3,4 Elisabeth M. Dykens,5 Daniel J. Driscoll,6 and Merlin G. Butler1 Purpose: Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are complex neurodevelopmental disor- ders caused by loss of expression of imprinted genes from the 15q11-q13 region depending on the parent of origin. Methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) kits from MRC- Holland (Amsterdam, The Netherlands) were used to detect PWS and AS deletion subtypes. We report our experience with two versions of the MS-MLPA-PWS/AS kit (original A1 and newer B1) in determining meth- ylation status and deletion subtypes in individuals with PWS. Methods: MS-MLPA analysis was performed on DNA isolated from a large cohort of PWS subjects with the MS-MLPA-PWS/AS-A1 and -B1 probe sets. Results: Both MS-MLPA kits will identify deletions in the 15q11-q13 region but the original MS-MLPA-A1 kit has a higher density of probes at the telomeric end of the 15q11-q13 region, which is more useful for identifying individuals with atypical deletions. The newer B1 kit contains more probes in the imprinting center (IC) and adjoining small noncoding RNAs useful in identifying small microdeletions. Conclusion: The A1 kit identified the typical deletions and smaller atypical deletions, whereas the B1 kit was more informative for identifying mi- crodeletions including the IC and SNORD116 regions.
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Milger Et Al. Pulmonary CCR2+CD4+ T Cells Are Immune Regulatory And
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