Migration of Thymic Pre-T Cells Regulates Development
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SRC Antibody - N-Terminal Region (ARP32476 P050) Data Sheet
SRC antibody - N-terminal region (ARP32476_P050) Data Sheet Product Number ARP32476_P050 Product Name SRC antibody - N-terminal region (ARP32476_P050) Size 50ug Gene Symbol SRC Alias Symbols ASV; SRC1; c-SRC; p60-Src Nucleotide Accession# NM_005417 Protein Size (# AA) 536 amino acids Molecular Weight 60kDa Product Format Lyophilized powder NCBI Gene Id 6714 Host Rabbit Clonality Polyclonal Official Gene Full Name V-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian) Gene Family SH2D This is a rabbit polyclonal antibody against SRC. It was validated on Western Blot by Aviva Systems Biology. At Aviva Systems Biology we manufacture rabbit polyclonal antibodies on a large scale (200-1000 Description products/month) of high throughput manner. Our antibodies are peptide based and protein family oriented. We usually provide antibodies covering each member of a whole protein family of your interest. We also use our best efforts to provide you antibodies recognize various epitopes of a target protein. For availability of antibody needed for your experiment, please inquire (). Peptide Sequence Synthetic peptide located within the following region: QTPSKPASADGHRGPSAAFAPAAAEPKLFGGFNSSDTVTSPQRAGPLAGG This gene is highly similar to the v-src gene of Rous sarcoma virus. This proto-oncogene may play a role in the Description of Target regulation of embryonic development and cell growth. SRC protein is a tyrosine-protein kinase whose activity can be inhibited by phosphorylation by c-SRC kinase. Mutations in this gene could be involved in the -
An Ancestral Role of Pericentrin in Centriole Formation Through SAS-6 Recruitment
bioRxiv preprint doi: https://doi.org/10.1101/313494; this version posted May 3, 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 The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. An ancestral role of pericentrin in centriole formation through SAS-6 recruitment Daisuke Ito1*, Sihem Zitouni1, Swadhin Chandra Jana1, Paulo Duarte1, Jaroslaw Surkont1, Zita Carvalho-Santos1,2, José B. Pereira-Leal1, Miguel Godinho Ferreira1,3 and Mónica Bettencourt-Dias1* 1. Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6, Oeiras 2780-156, Portugal. 2. Present address: Champalimaud Centre for the Unknown, Lisbon, Portugal 3. Institute for Research on Cancer and Aging of Nice (IRCAN), INSERM U1081 UMR7284 CNRS, 06107 Nice, France *Correspondence to: [email protected] (DI); [email protected] (MBD) Running title: Ancestral role of pericentrin-SAS-6 interaction Key words: centrosome, centriole, fission yeast, SPB, SAS-6, pericentrin, calmodulin, evolution Short summary The pericentriolar matrix (PCM) is not only important for microtubule-nucleation but also can regulate centriole biogenesis. Ito et al. reveal an ancestral interaction between the centriole protein SAS-6 and the PCM component pericentrin, which regulates centriole biogenesis and elongation. 1 bioRxiv preprint doi: https://doi.org/10.1101/313494; this version posted May 3, 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 The centrosome is composed of two centrioles surrounded by a microtubule-nucleating pericentriolar matrix (PCM). Centrioles regulate matrix assembly. Here we ask whether the matrix also regulates centriole assembly. -
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. -
Identification of Genes Concordantly Expressed with Atoh1 During Inner Ear Development
Original Article doi: 10.5115/acb.2011.44.1.69 pISSN 2093-3665 eISSN 2093-3673 Identification of genes concordantly expressed with Atoh1 during inner ear development Heejei Yoon, Dong Jin Lee, Myoung Hee Kim, Jinwoong Bok Department of Anatomy, Brain Korea 21 Project for Medical Science, College of Medicine, Yonsei University, Seoul, Korea Abstract: The inner ear is composed of a cochlear duct and five vestibular organs in which mechanosensory hair cells play critical roles in receiving and relaying sound and balance signals to the brain. To identify novel genes associated with hair cell differentiation or function, we analyzed an archived gene expression dataset from embryonic mouse inner ear tissues. Since atonal homolog 1a (Atoh1) is a well known factor required for hair cell differentiation, we searched for genes expressed in a similar pattern with Atoh1 during inner ear development. The list from our analysis includes many genes previously reported to be involved in hair cell differentiation such as Myo6, Tecta, Myo7a, Cdh23, Atp6v1b1, and Gfi1. In addition, we identified many other genes that have not been associated with hair cell differentiation, including Tekt2, Spag6, Smpx, Lmod1, Myh7b, Kif9, Ttyh1, Scn11a and Cnga2. We examined expression patterns of some of the newly identified genes using real-time polymerase chain reaction and in situ hybridization. For example, Smpx and Tekt2, which are regulators for cytoskeletal dynamics, were shown specifically expressed in the hair cells, suggesting a possible role in hair cell differentiation or function. Here, by re- analyzing archived genetic profiling data, we identified a list of novel genes possibly involved in hair cell differentiation. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Systematic Description of the Expression and Prognostic Value of M6A Regulators in Human Ovarian Cancer
Systematic Description of the Expression and Prognostic Value of M6A Regulators in Human Ovarian Cancer Yuwei Chen Fujian Medical University Fujian Cancer Hospital Yang Sun ( [email protected] ) Fujian Cancer Hospital https://orcid.org/0000-0003-4224-8832 Xinbei Chen Fujian Medical University Fujian Cancer Hospital Siming Li Fujian Medical University Fujian Cancer Hospital Hongmei Xia Fujian Cancer Hospital Research Keywords: m6A regulators, m6A, ovarian cancer, Prognostic values, bioinformatics analysis. Posted Date: December 22nd, 2020 DOI: https://doi.org/10.21203/rs.3.rs-131682/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Systematic description of the expression and prognostic value of m6A regulators in human ovarian cancer 1 Yuwei Chen1, Yang Sun1*, Xinbei Chen1, Siming Li1, Hongmei Xia1 2 * Correspondence: 3 Yang Sun 4 [email protected] 5 Total words:5253 6 Total Figures and Tables: 11 Figures and 3 Tables 7 Keywords: m6A regulators, m6A, ovarian cancer, Prognostic values, 8 bioinformatics analysis. 9 Abstract 10 Background: N6-methyladenine (m6A) methylation, known as a kind of RNA 11 methylation regulator, has become a hotspot for research in the life sciences in recent 12 years. The existing studies revealed that m6A regulators helped to regulate the 13 progression of several malignant tumors. However, the expression mode and 14 prognostic value of m6A regulators in ovarian cancer have not been fully elucidated. 15 Methods: ONCOMINE, GEPIA, Human protein atlas, Kaplan-meier, UALCAN, 16 cBioPortal, GeneMANIA, DAVID, Sring, and Metascape were utilized in this study. 17 Results: In this study, through a comprehensive use of multiple database systems, 18 m6A regulators-induced mRNA and protein expression levels and their prognostic 19 value in the epithelial ovarian cancer of various histological types were analyzed. -
A Novel Hypoxic Long Noncoding RNA KB-1980E6.3 Maintains Breast Cancer Stem Cell Stemness Via Interacting with IGF2BP1 to Facilitate C-Myc Mrna Stability
Oncogene (2021) 40:1609–1627 https://doi.org/10.1038/s41388-020-01638-9 ARTICLE A novel hypoxic long noncoding RNA KB-1980E6.3 maintains breast cancer stem cell stemness via interacting with IGF2BP1 to facilitate c-Myc mRNA stability 1 2 3 4 1 1 1 1 1 Pengpeng Zhu ● Fang He ● Yixuan Hou ● Gang Tu ● Qiao Li ● Ting Jin ● Huan Zeng ● Yilu Qin ● Xueying Wan ● 1 1 5 1 Yina Qiao ● Yuxiang Qiu ● Yong Teng ● Manran Liu Received: 15 June 2020 / Revised: 13 November 2020 / Accepted: 18 December 2020 / Published online: 19 January 2021 © The Author(s), under exclusive licence to Springer Nature Limited 2021. This article is published with open access Abstract The hostile hypoxic microenvironment takes primary responsibility for the rapid expansion of breast cancer tumors. However, the underlying mechanism is not fully understood. Here, using RNA sequencing (RNA-seq) analysis, we identified a hypoxia-induced long noncoding RNA (lncRNA) KB-1980E6.3, which is aberrantly upregulated in clinical breast cancer tissues and closely correlated with poor prognosis of breast cancer patients. The enhanced lncRNA KB- 1980E6.3 facilitates breast cancer stem cells (BCSCs) self-renewal and tumorigenesis under hypoxic microenvironment both 1234567890();,: 1234567890();,: in vitro and in vivo. Mechanistically, lncRNA KB-1980E6.3 recruited insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) to form a lncRNA KB-1980E6.3/IGF2BP1/c-Myc signaling axis that retained the stability of c-Myc mRNA through increasing binding of IGF2BP1 with m6A-modified c-Myc coding region instability determinant (CRD) mRNA. In conclusion, we confirm that lncRNA KB-1980E6.3 maintains the stemness of BCSCs through lncRNA KB-1980E6.3/ IGF2BP1/c-Myc axis and suggest that disrupting this axis might provide a new therapeutic target for refractory hypoxic tumors. -
Supplementary Table S1. Correlation Between the Mutant P53-Interacting Partners and PTTG3P, PTTG1 and PTTG2, Based on Data from Starbase V3.0 Database
Supplementary Table S1. Correlation between the mutant p53-interacting partners and PTTG3P, PTTG1 and PTTG2, based on data from StarBase v3.0 database. PTTG3P PTTG1 PTTG2 Gene ID Coefficient-R p-value Coefficient-R p-value Coefficient-R p-value NF-YA ENSG00000001167 −0.077 8.59e-2 −0.210 2.09e-6 −0.122 6.23e-3 NF-YB ENSG00000120837 0.176 7.12e-5 0.227 2.82e-7 0.094 3.59e-2 NF-YC ENSG00000066136 0.124 5.45e-3 0.124 5.40e-3 0.051 2.51e-1 Sp1 ENSG00000185591 −0.014 7.50e-1 −0.201 5.82e-6 −0.072 1.07e-1 Ets-1 ENSG00000134954 −0.096 3.14e-2 −0.257 4.83e-9 0.034 4.46e-1 VDR ENSG00000111424 −0.091 4.10e-2 −0.216 1.03e-6 0.014 7.48e-1 SREBP-2 ENSG00000198911 −0.064 1.53e-1 −0.147 9.27e-4 −0.073 1.01e-1 TopBP1 ENSG00000163781 0.067 1.36e-1 0.051 2.57e-1 −0.020 6.57e-1 Pin1 ENSG00000127445 0.250 1.40e-8 0.571 9.56e-45 0.187 2.52e-5 MRE11 ENSG00000020922 0.063 1.56e-1 −0.007 8.81e-1 −0.024 5.93e-1 PML ENSG00000140464 0.072 1.05e-1 0.217 9.36e-7 0.166 1.85e-4 p63 ENSG00000073282 −0.120 7.04e-3 −0.283 1.08e-10 −0.198 7.71e-6 p73 ENSG00000078900 0.104 2.03e-2 0.258 4.67e-9 0.097 3.02e-2 Supplementary Table S2. -
Cell Cycle Control of Spindle Pole Body Duplication and Splitting by Sfi1 and Cdc31 in Fission Yeast
ß 2015. Published by The Company of Biologists Ltd | Journal of Cell Science (2015) 128, 1481–1493 doi:10.1242/jcs.159657 RESEARCH ARTICLE Cell cycle control of spindle pole body duplication and splitting by Sfi1 and Cdc31 in fission yeast Ime`ne B. Bouhlel1,2,§, Midori Ohta3,*,§, Adeline Mayeux1,2,§, Nicole Bordes1,2, Florent Dingli1, Je´roˆ me Boulanger1,2, Guilhem Velve Casquillas1,2,`, Damarys Loew1, Phong T. Tran1,2, Masamitsu Sato3 and Anne Paoletti1,2," ABSTRACT Spindle pole bodies (SPBs) are yeast plaque-like organelles attached to the nuclear envelope that are functionally similar to Spindle pole biogenesis and segregation are tightly coordinated to centrosomes of animal cells. Like centrosomes, they are produce a bipolar mitotic spindle. In yeasts, the spindle pole body generated by conservative duplication of pre-existing SPBs. In (SPB) half-bridge composed of Sfi1 and Cdc31 duplicates to budding as well as fission yeast, the daughter SPB assembles at promote the biogenesis of a second SPB. Sfi1 accumulates at the the tip of a mother SPB appendage called the bridge, which half-bridge in two phases in Schizosaccharomyces pombe, from maintains the association of the duplicated SPBs until mitotic anaphase to early septation and throughout G2 phase. We found onset. Duplicated SPBs inserted in the nuclear envelope nucleate that the function of Sfi1–Cdc31 in SPB duplication is accomplished intranuclear microtubules to initiate bipolar spindle assembly before septation ends and G2 accumulation starts. Thus, Sfi1 early (Adams and Kilmartin, 2000; Ding et al., 1997; Jaspersen and accumulation at mitotic exit might correspond to half-bridge Ghosh, 2012; Jaspersen and Winey, 2004; Lim et al., 2009; duplication. -