INPP5D (Phospho Y1021) Polyclonal Antibody

Total Page：16

File Type：pdf, Size：1020Kb

INPP5D (Phospho Y1021) Polyclonal Antibody

INPP5D (phospho Y1021) polyclonal Gene Alias: MGC104855, MGC142140, MGC142142, antibody SHIP, SHIP1, SIP-145, hp51CN Gene Summary: This gene is a member of the inositol Catalog Number: PAB31642 polyphosphate-5-phosphatase (INPP5) family and Regulation Status: For research use only (RUO) encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein Product Description: Rabbit polyclonal antibody raised interaction domains. Expression of this protein is against synthetic peptide of human INPP5D (phospho restricted to hematopoietic cells where its movement Y1021). from the cytosol to the plasma membrane is mediated by tyrosine phosphorylation. At the plasma membrane, the Immunogen: A synthetic peptide corresponding to protein hydrolyzes the 5' phosphate from amino acids 960-1040 of human INPP5D (phospho phosphatidylinositol (3,4,5)-trisphosphate and Y1021). inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. Overall, the protein Host: Rabbit functions as a negative regulator of myeliod cell proliferation and survival. Alternate transcriptional splice Reactivity: Human,Mouse,Rat variants, encoding different isoforms, have been characterized. [provided by RefSeq] Applications: ELISA, WB-Ce (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Specificity: This antibody detects endogenous levels of INPP5D protein only when phosphorylated at Y1021. Form: Liquid Purification: Affinity purification Isotype: IgG Recommend Usage: ELISA (1:40000) Western Blot (1:500-2000) The optimal working dilution should be determined by the end user. Storage Buffer: In PBS (50% glycerol, 0.5% BSA and 0.02% sodium azide). Storage Instruction: Store at -20°C. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 3635 Gene Symbol: INPP5D Page 1/1 Powered by TCPDF (www.tcpdf.org).

Copy Link

Recommended publications

Hypoxia-Induced P53 Modulates Both Apoptosis and Radiosensitivity Via AKT
Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT Katarzyna B. Leszczynska, … , Francesca M. Buffa, Ester M. Hammond J Clin Invest. 2015;125(6):2385-2398. https://doi.org/10.1172/JCI80402. Research Article Oncology Restoration of hypoxia-induced apoptosis in tumors harboring p53 mutations has been proposed as a potential therapeutic strategy; however, the transcriptional targets that mediate hypoxia-induced p53-dependent apoptosis remain elusive. Here, we demonstrated that hypoxia-induced p53-dependent apoptosis is reliant on the DNA-binding and transactivation domains of p53 but not on the acetylation sites K120 and K164, which, in contrast, are essential for DNA damage–induced, p53-dependent apoptosis. Evaluation of hypoxia-induced transcripts in multiple cell lines identified a group of genes that are hypoxia-inducible proapoptotic targets of p53, including inositol polyphosphate-5-phosphatase (INPP5D), pleckstrin domain–containing A3 (PHLDA3), sulfatase 2 (SULF2), B cell translocation gene 2 (BTG2), cytoplasmic FMR1-interacting protein 2 (CYFIP2), and KN motif and ankyrin repeat domains 3 (KANK3). These targets were also regulated by p53 in human cancers, including breast, brain, colorectal, kidney, bladder, and melanoma cancers. Downregulation of these hypoxia-inducible targets associated with poor prognosis, suggesting that hypoxia-induced apoptosis contributes to p53-mediated tumor suppression and treatment response. Induction of p53 targets, PHLDA3, and a specific INPP5D transcript mediated apoptosis in response to hypoxia through AKT inhibition. Moreover, pharmacological inhibition of AKT led to apoptosis in the hypoxic regions of p53-deficient tumors and consequently increased radiosensitivity. Together, these results identify mediators of hypoxia-induced p53-dependent apoptosis and suggest AKT inhibition may improve radiotherapy response in p53-deficient tumors.
[Show full text]
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Proﬁle of Tumor-Speciﬁc CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.
[Show full text]
Influence on the Transcriptome of Tec Family Kinases with Special Emphasis on Btk
From Department of Laboratory Medicine Karolinska Institutet, Stockholm, Sweden INFLUENCE ON THE TRANSCRIPTOME OF TEC FAMILY KINASES WITH SPECIAL EMPHASIS ON BTK Hossain M. Nawaz Stockholm 2013 All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by E-print AB 2013 © Hossain Nawaz, 2013 ISBN 978-91-7549-311-4 Science is a way of thinking much more than it is a body of knowledge. Carl Sagan (1934-1996), American Scientist To my family ABSTRACT Over the last decade, scientists all over the world have profoundly used gene expression profiling based on microarray. Affymetrix is considered as the one of the pioneer platforms in the field of microarray technology. In this thesis, the Affymetrix Genechip® arrays were used to study the transcriptome of Tec family kinases with special emphasis on Bruton’s tyrosine kinase (Btk) in avian B-lymphoma DT40 cell- line and fruit flies (Drosophila melanogaster). Btk is a protein tyrosine kinase belonging to the Tec family of kinases (TFKs). Btk is involved in signal transduction of the B cell receptor (BCR) pathway and plays an essential role in B lymphocyte development and function. X-linked agammaglobulinemia (XLA) is a primary immunodeficiency disease caused by mutations in the BTK gene. We studied Btk- deficient DT40 avian cell line reconstituted with the human BTK gene in order to investigate whether the loss-of-function can be rescued by the gene substitution at the transcriptomic level. Differences in the gene expression pattern showed statistically significant changes between parental DT40 and all the Btk KO cell populations, irrespective of whether they are reconstituted or not.
[Show full text]
CD22 Mouse Monoclonal Antibody [Clone ID: OTI2A4] – TA807831
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 TA807831 CD22 Mouse Monoclonal Antibody [Clone ID: OTI2A4] Product data: Product Type: Primary Antibodies Clone Name: OTI2A4 Applications: WB Recommended Dilution: WB 1:2000 Reactivity: Human Host: Mouse Isotype: IgG1 Clonality: Monoclonal Immunogen: Human recombinant protein fragment corresponding to amino acids 707-847 of human CD22(NP_001762) produced in E.coli. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Gene Name: CD22 molecule Database Link: NP_001762 Entrez Gene 933 Human P20273 Background: Predominantly monomer of isoform CD22-beta. Also found as heterodimer of isoform CD22- beta and a shorter isoform. Interacts with PTPN6/SHP-1, LYN, SYK, PIK3R1/PIK3R2 and PLCG1 upon phosphorylation. Interacts with GRB2, INPP5D and SHC1 upon phosphorylation (By similarity). May form a complex with INPP5D/SHIP, GRB2 and SHC1. [UniProtKB/Swiss-Prot Function] Synonyms: SIGLEC-2; SIGLEC2 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 CD22 Mouse Monoclonal Antibody [Clone ID: OTI2A4] – TA807831 Protein Families: Druggable Genome, Transmembrane Protein Pathways: B cell receptor signaling pathway, Cell adhesion molecules (CAMs), Hematopoietic cell lineage Product images: HEK293T cells were transfected with the pCMV6- ENTRY control (Left lane) or pCMV6-ENTRY CD22 ([RC216939], Right lane) cDNA for 48 hrs and lysed.
[Show full text]
The Tec Kinase−Regulated Phosphoproteome Reveals a Mechanism for the Regulation of Inhibitory Signals in Murine Macrophages
The Tec Kinase−Regulated Phosphoproteome Reveals a Mechanism for the Regulation of Inhibitory Signals in Murine Macrophages This information is current as Giacomo Tampella, Hannah M. Kerns, Deqiang Niu, Swati of September 29, 2021. Singh, Socheath Khim, Katherine A. Bosch, Meghan E. Garrett, Albanus Moguche, Erica Evans, Beth Browning, Tahmina A. Jahan, Mariana Nacht, Alejandro Wolf-Yadlin, Alessandro Plebani, Jessica A. Hamerman, David J. Rawlings and Richard G. James Downloaded from J Immunol published online 29 May 2015 http://www.jimmunol.org/content/early/2015/05/29/jimmun ol.1403238 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2015/05/29/jimmunol.140323 Material 8.DCSupplemental Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 29, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published May 29, 2015, doi:10.4049/jimmunol.1403238 The Journal of Immunology The Tec Kinase–Regulated Phosphoproteome Reveals a Mechanism for the Regulation of Inhibitory Signals in Murine Macrophages Giacomo Tampella,*,1 Hannah M.
[Show full text]
HHS Public Access Author Manuscript
HHS Public Access Author manuscript Author Manuscript Author ManuscriptBreast Cancer Author Manuscript Res Treat Author Manuscript . Author manuscript; available in PMC 2016 June 01. Published in final edited form as: Breast Cancer Res Treat. 2015 June ; 151(2): 453–463. doi:10.1007/s10549-015-3401-8. Body mass index associated with genome-wide methylation in breast tissue Brionna Y. Hair1, Zongli Xu2, Erin L. Kirk1, Sophia Harlid2, Rupninder Sandhu3, Whitney R. Robinson1,3, Michael C. Wu4, Andrew F. Olshan1, Kathleen Conway1,3, Jack A. Taylor2, and Melissa A. Troester1 1 Department of Epidemiology, University of North Carolina at Chapel Hill, CB #7435, 2101 McGavran-Greenberg Hall, Chapel Hill, NC 27599-7435, USA 2 Epidemiology Branch, and Epigenomics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences (NIH), Research Triangle Park, NC, USA 3 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA 4 Fred Hutchinson Cancer Research Center, Seattle, WA, USA Abstract Gene expression studies indicate that body mass index (BMI) is associated with molecular pathways involved in inflammation, insulin-like growth factor activation, and other carcinogenic processes in breast tissue. The goal of this study was to determine whether BMI is associated with gene methylation in breast tissue and to identify pathways that are commonly methylated in association with high BMI. Epigenome-wide methylation profiles were determined using the Illumina HumanMethylation450 BeadChip array in the non-diseased breast tissue of 81 women undergoing breast surgery between 2009 and 2013 at the University of North Carolina Hospitals. Multivariable, robust linear regression was performed to identify methylation sites associated with BMI at a false discovery rate q value <0.05.
[Show full text]
Novel Alzheimer Risk Genes Determine the Microglia Response To
bioRxiv preprint doi: https://doi.org/10.1101/491902; this version posted December 11, 2018. 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. Title Page Novel Alzheimer risk genes determine the microglia response to amyloid-β but not to TAU pathology Annerieke Sierksma, PhD1,2,3, Ashley Lu, MSc1,2,3, Evgenia Salta, PhD2,3, Renzo Mancuso, PhD2,3, Jesus Zoco, MSc2,3, David Blum, PhD4, Prof Luc Buée, PhD4, Prof Bart De Strooper, PhD2,3,5,6, Mark Fiers, PhD2,3,6 Affiliations 1. These authors contributed equally 2. VIB Center for Brain & Disease Research, Leuven, Belgium 3. KU Leuven, Department of Neurosciences, Leuven research Institute for Neuroscience and Disease (LIND), Leuven, Belgium 4. Université Lille, INSERM, CHU Lille, LabEx DISTALZ, UMR-S 1172, Alzheimer & Tauopathies, Lille, France 5. Dementia Research Institute, ION, University College London, London, UK 6. Senior and corresponding authors Contact: Dr. Mark Fiers & Prof. Bart De Strooper, VIB - Center for Brain & Disease Research, KU Leuven - Department of Neurosciences, O&N4, Herestraat 49 box 602 Leuven, Belgium. E-mail: [email protected]; [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/491902; this version posted December 11, 2018. 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. Abstract Background: Thousands of SNPs associated with risk of Alzheimer’s disease (AD) in genome-wide association studies (GWAS) do not reach genome-wide significance.
[Show full text]
Human CD Marker Chart Reviewed by HLDA1 Bdbiosciences.Com/Cdmarkers
BD Biosciences Human CD Marker Chart Reviewed by HLDA1 bdbiosciences.com/cdmarkers 23-12399-01 CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD1a R4, T6, Leu6, HTA1 b-2-Microglobulin, CD74 + + + – + – – – CD93 C1QR1,C1qRP, MXRA4, C1qR(P), Dj737e23.1, GR11 – – – – – + + – – + – CD220 Insulin receptor (INSR), IR Insulin, IGF-2 + + + + + + + + + Insulin-like growth factor 1 receptor (IGF1R), IGF-1R, type I IGF receptor (IGF-IR), CD1b R1, T6m Leu6 b-2-Microglobulin + + + – + – – – CD94 KLRD1, Kp43 HLA class I, NKG2-A, p39 + – + – – – – – – CD221 Insulin-like growth factor 1 (IGF-I), IGF-II, Insulin JTK13 + + + + + + + + + CD1c M241, R7, T6, Leu6, BDCA1 b-2-Microglobulin + + + – + – – – CD178, FASLG, APO-1, FAS, TNFRSF6, CD95L, APT1LG1, APT1, FAS1, FASTM, CD95 CD178 (Fas ligand) + + + + + – – IGF-II, TGF-b latency-associated peptide (LAP), Proliferin, Prorenin, Plasminogen, ALPS1A, TNFSF6, FASL Cation-independent mannose-6-phosphate receptor (M6P-R, CIM6PR, CIMPR, CI- CD1d R3G1, R3 b-2-Microglobulin, MHC II CD222 Leukemia
[Show full text]
Systematic Elucidation of Neuron-Astrocyte Interaction in Models of Amyotrophic Lateral Sclerosis Using Multi-Modal Integrated Bioinformatics Workflow
ARTICLE https://doi.org/10.1038/s41467-020-19177-y OPEN Systematic elucidation of neuron-astrocyte interaction in models of amyotrophic lateral sclerosis using multi-modal integrated bioinformatics workflow Vartika Mishra et al.# 1234567890():,; Cell-to-cell communications are critical determinants of pathophysiological phenotypes, but methodologies for their systematic elucidation are lacking. Herein, we propose an approach for the Systematic Elucidation and Assessment of Regulatory Cell-to-cell Interaction Net- works (SEARCHIN) to identify ligand-mediated interactions between distinct cellular com- partments. To test this approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor neurons (MNs) by an unknown mechanism. Our integrative analysis that combines proteomics and regulatory network analysis infers the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligand-receptor pair. The inferred deleterious role of APP and DR6 is confirmed in vitro in models of ALS. Moreover, the DR6 knockdown in MNs of transgenic mutSOD1 mice attenuates the ALS-like phenotype. Our results support the usefulness of integrative, systems biology approach to gain insights into complex neurobiological disease processes as in ALS and posit that the proposed methodology is not restricted to this biological context and could be used in a variety of other non-cell-autonomous communication
[Show full text]
INPP5D Monoclonal Antibody, Clone SHIP-02
INPP5D monoclonal antibody, clone Gene Symbol: INPP5D SHIP-02 Gene Alias: MGC104855, MGC142140, MGC142142, SHIP, SHIP1, SIP-145, hp51CN Catalog Number: MAB3646 Gene Summary: This gene is a member of the inositol Regulatory Status: For research use only (RUO) polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an Product Description: Mouse monoclonal antibody inositol phosphatase domain, and two C-terminal protein raised against synthetic peptide of INPP5D. interaction domains. Expression of this protein is Clone Name: SHIP-02 restricted to hematopoietic cells where its movement from the cytosol to the plasma membrane is mediated by Immunogen: A synthetic peptide corresponding to tyrosine phosphorylation. At the plasma membrane, the N-terminus human INPP5D. protein hydrolyzes the 5' phosphate from phosphatidylinositol (3,4,5)-trisphosphate and Host: Mouse inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. Overall, the protein Theoretical MW (kDa): 110, 125, 130, 135, functions as a negative regulator of myeliod cell proliferation and survival. Alternate transcriptional splice Reactivity: Human variants, encoding different isoforms, have been characterized. [provided by RefSeq] Applications: Flow Cyt, WB-Ce (See our web site product page for detailed applications References: information) 1. Tissue expression and enzymologic characterization of human prostate specific membrane antigen and its rat Protocols: See our web site at and pig orthologs. Rovenska M, Hlouchova K, Sacha P, http://www.abnova.com/support/protocols.asp or product Mlcochova P, Horak V, Zamecnik J, Barinka C, page for detailed protocols Konvalinka J. Prostate. 2008 Feb 1;68(2):171-82. Specificity: This antibody reacts with SHIP-1, a 2.
[Show full text]
Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared Amongst Δγ T, Innate Lymphoid, and Th Cells
Downloaded from http://www.jimmunol.org/ by guest on September 26, 2021 δγ is online at: average * The Journal of Immunology , 10 of which you can access for free at: 2016; 197:1460-1470; Prepublished online 6 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600643 http://www.jimmunol.org/content/197/4/1460 Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared amongst T, Innate Lymphoid, and Th Cells You Jeong Lee, Gabriel J. Starrett, Seungeun Thera Lee, Rendong Yang, Christine M. Henzler, Stephen C. Jameson and Kristin A. Hogquist J Immunol cites 41 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2016/07/06/jimmunol.160064 3.DCSupplemental This article http://www.jimmunol.org/content/197/4/1460.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 26, 2021. The Journal of Immunology Lineage-Speciﬁc Effector Signatures of Invariant NKT Cells Are Shared amongst gd T, Innate Lymphoid, and Th Cells You Jeong Lee,* Gabriel J.
[Show full text]
HLA-DPA1 Gene Is a Potential Predictor with Prognostic Values in Multiple Myeloma Jie Yang, Fei Wang and Baoan Chen*
Yang et al. BMC Cancer (2020) 20:915 https://doi.org/10.1186/s12885-020-07393-0 RESEARCH ARTICLE Open Access HLA-DPA1 gene is a potential predictor with prognostic values in multiple myeloma Jie Yang, Fei Wang and Baoan Chen* Abstract Background: Multiple myeloma (MM) is an incurable hematological tumor, which is closely related to hypoxic bone marrow microenvironment. However, the underlying mechanisms are still far from fully understood. We took integrated bioinformatics analysis with expression profile GSE110113 downloaded from National Center for Biotechnology Information-Gene Expression Omnibus (NCBI-GEO) database, and screened out major histocompatibility complex, class II, DP alpha 1 (HLA-DPA1) as a hub gene related to hypoxia in MM. Methods: Differentially expressed genes (DEGs) were filtrated with R package “limma”. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were performed using “clusterProfiler” package in R. Then, protein-protein interaction (PPI) network was established. Hub genes were screened out according to Maximal Clique Centrality (MCC). PrognoScan evaluated all the significant hub genes for survival analysis. ScanGEO was used for visualization of gene expression in different clinical studies. P and Cox p value < 0.05 was considered to be statistical significance. Results: HLA-DPA1 was finally picked out as a hub gene in MM related to hypoxia. MM patients with down-regulated expression of HLA-DPA1 has statistically significantly shorter disease specific survival (DSS) (COX p = 0.005411). Based on the clinical data of GSE47552 dataset, HLA-DPA1 expression showed significantly lower in MM patients than that in healthy donors (HDs) (p = 0.017).
[Show full text]