TMEM123 Antibody

Total Page:16

File Type:pdf, Size:1020Kb

TMEM123 Antibody Product Datasheet TMEM123 Antibody Catalog No: #40063 Orders: [email protected] Description Support: [email protected] Product Name TMEM123 Antibody Host Species Rabbit Clonality Polyclonal Purification Antigen affinity purification. Applications IHC Species Reactivity Hu Specificity The antibody detects endogenous levels of total TMEM123 protein. Immunogen Type Protein Immunogen Description Fusion protein corresponding to a region derived from internal residues of human transmembrane protein 123 Target Name TMEM123 Other Names KCT3; PORMIN; PORIMIN Accession No. Swiss-Prot:Q8N131Gene Accssion:BC032296 Concentration 1.3mg/ml Formulation Rabbit IgG in pH7.4 PBS, 0.05% NaN3, 40% Glycerol. Storage Store at -20°C Application Details Immunohistochemistry: 1:100-1:200 Images Immunohistochemical analysis of paraffin-embedded Human Esophagus cancer tissue using #40063 at dilution 1/200. Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 1 Immunohistochemical analysis of paraffin-embedded Human Liver cancer tissue using #40063 at dilution 1/200. Background This gene encodes a highly glycosylated transmembrane protein with a high content of threonine and serine residues in its extracellular domain, similar to a broadly defined category of proteins termed mucins. Exposure of some cell types to anti-PORIMIN (pro-oncosis receptor inducing membrane injury) antibody, crosslinks this protein on the cell surface and induces a type of cell death termed oncosis. Oncosis is distinct from apoptosis and is characterized by a loss of cell membrane integrity without DNA fragmentation. This gene product is proposed to function as a cell surface receptor that mediates cell death. 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.
Recommended publications
  • Bilateral Gene Interaction Hierarchy Analysis of the Cell Death Gene
    White et al. BMC Genomics (2016) 17:130 DOI 10.1186/s12864-016-2412-0 RESEARCH ARTICLE Open Access Bilateral gene interaction hierarchy analysis of the cell death gene response emphasizes the significance of cell cycle genes following unilateral traumatic brain injury Todd E. White1, Monique C. Surles-Zeigler1, Gregory D. Ford2, Alicia S. Gates1, Benem Davids1, Timothy Distel1,4, Michelle C. LaPlaca3 and Byron D. Ford1,4* Abstract Background: Delayed or secondary cell death that is caused by a cascade of cellular and molecular processes initiated by traumatic brain injury (TBI) may be reduced or prevented if an effective neuroprotective strategy is employed. Microarray and subsequent bioinformatic analyses were used to determine which genes, pathways and networks were significantly altered 24 h after unilateral TBI in the rat. Ipsilateral hemi-brain, the corresponding contralateral hemi-brain, and naïve (control) brain tissue were used for microarray analysis. Results: Ingenuity Pathway Analysis showed cell death and survival (CD) to be a top molecular and cellular function associated with TBI on both sides of the brain. One major finding was that the overall gene expression pattern suggested an increase in CD genes in ipsilateral brain tissue and suppression of CD genes contralateral to the injury which may indicate an endogenous protective mechanism. We created networks of genes of interest (GOI) and ranked the genes by the number of direct connections each had in the GOI networks, creating gene interaction hierarchies (GIHs). Cell cycle was determined from the resultant GIHs to be a significant molecular and cellular function in post-TBI CD gene response.
    [Show full text]
  • Involvement of DPP9 in Gene Fusions in Serous Ovarian Carcinoma
    Smebye et al. BMC Cancer (2017) 17:642 DOI 10.1186/s12885-017-3625-6 RESEARCH ARTICLE Open Access Involvement of DPP9 in gene fusions in serous ovarian carcinoma Marianne Lislerud Smebye1,2, Antonio Agostini1,2, Bjarne Johannessen2,3, Jim Thorsen1,2, Ben Davidson4,5, Claes Göran Tropé6, Sverre Heim1,2,5, Rolf Inge Skotheim2,3 and Francesca Micci1,2* Abstract Background: A fusion gene is a hybrid gene consisting of parts from two previously independent genes. Chromosomal rearrangements leading to gene breakage are frequent in high-grade serous ovarian carcinomas and have been reported as a common mechanism for inactivating tumor suppressor genes. However, no fusion genes have been repeatedly reported to be recurrent driver events in ovarian carcinogenesis. We combined genomic and transcriptomic information to identify novel fusion gene candidates and aberrantly expressed genes in ovarian carcinomas. Methods: Examined were 19 previously karyotyped ovarian carcinomas (18 of the serous histotype and one undifferentiated). First, karyotypic aberrations were compared to fusion gene candidates identified by RNA sequencing (RNA-seq). In addition, we used exon-level gene expression microarrays as a screening tool to identify aberrantly expressed genes possibly involved in gene fusion events, and compared the findings to the RNA-seq data. Results: We found a DPP9-PPP6R3 fusion transcript in one tumor showing a matching genomic 11;19-translocation. Another tumor had a rearrangement of DPP9 with PLIN3. Both rearrangements were associated with diminished expression of the 3′ end of DPP9 corresponding to the breakpoints identified by RNA-seq. For the exon-level expression analysis, candidate fusion partner genes were ranked according to deviating expression compared to the median of the sample set.
    [Show full text]
  • Modulating Hallmarks of Cholangiocarcinoma
    University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Fall 12-14-2018 Modulating Hallmarks of Cholangiocarcinoma Cody Wehrkamp University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Molecular Biology Commons Recommended Citation Wehrkamp, Cody, "Modulating Hallmarks of Cholangiocarcinoma" (2018). Theses & Dissertations. 337. https://digitalcommons.unmc.edu/etd/337 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. MODULATING HALLMARKS OF CHOLANGIOCARCINOMA by Cody J. Wehrkamp A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor Justin L. Mott University of Nebraska Medical Center Omaha, Nebraska November 2018 Supervisory Committee: Kaustubh Datta, Ph.D. Melissa Teoh‐Fitzgerald, Ph.D. Richard G. MacDonald, Ph.D. Acknowledgements This endeavor has led to scientific as well as personal growth for me. I am indebted to many for their knowledge, influence, and support along the way. To my mentor, Dr. Justin L. Mott, you have been an incomparable teacher and invaluable guide. You upheld for me the concept that science is intrepid, even when the experience is trying. Through my training, and now here at the end, I can say that it has been an honor to be your protégé. When you have shaped your future graduates to be and do great, I will be privileged to say that I was your first one.
    [Show full text]
  • A Genome-Wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis
    bioRxiv preprint doi: https://doi.org/10.1101/2020.06.05.136192; this version posted June 6, 2020. 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. Contreras et al., A Genome-wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis Ximena Contreras1, Amarbayasgalan Davaatseren1, Nicole Amberg1, Andi H. Hansen1, Johanna Sonntag1, Lill Andersen2, Tina Bernthaler2, Anna Heger1, Randy Johnson3, Lindsay A. Schwarz4,5, Liqun Luo4, Thomas Rülicke2 & Simon Hippenmeyer1,6,# 1 Institute of Science and Technology Austria, Am Campus 1, 3400 Klosterneuburg, Austria 2 Institute of Laboratory Animal Science, University of Veterinary Medicine Vienna, Vienna, Austria 3 Department of Biochemistry and Molecular Biology, University of Texas, Houston, TX 77030, USA 4 HHMI and Department of Biology, Stanford University, Stanford, CA 94305, USA 5 Present address: St. Jude Children’s Research Hospital, Memphis, TN 38105, USA 6 Lead contact #Correspondence and requests for materials should be addressed to S.H. ([email protected]) 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.06.05.136192; this version posted June 6, 2020. 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. Contreras et al., SUMMARY Mosaic Analysis with Double Markers (MADM) offers a unique approach to visualize and concomitantly manipulate genetically-defined cells in mice with single-cell resolution.
    [Show full text]
  • Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
    Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement.
    [Show full text]
  • Pan-Cancer Analysis of Homozygous Deletions in Primary Tumours Uncovers Rare Tumour Suppressors
    Corrected: Author correction; Corrected: Author correction ARTICLE DOI: 10.1038/s41467-017-01355-0 OPEN Pan-cancer analysis of homozygous deletions in primary tumours uncovers rare tumour suppressors Jiqiu Cheng1,2, Jonas Demeulemeester 3,4, David C. Wedge5,6, Hans Kristian M. Vollan2,3, Jason J. Pitt7,8, Hege G. Russnes2,9, Bina P. Pandey1, Gro Nilsen10, Silje Nord2, Graham R. Bignell5, Kevin P. White7,11,12,13, Anne-Lise Børresen-Dale2, Peter J. Campbell5, Vessela N. Kristensen2, Michael R. Stratton5, Ole Christian Lingjærde 10, Yves Moreau1 & Peter Van Loo 3,4 1234567890 Homozygous deletions are rare in cancers and often target tumour suppressor genes. Here, we build a compendium of 2218 primary tumours across 12 human cancer types and sys- tematically screen for homozygous deletions, aiming to identify rare tumour suppressors. Our analysis defines 96 genomic regions recurrently targeted by homozygous deletions. These recurrent homozygous deletions occur either over tumour suppressors or over fragile sites, regions of increased genomic instability. We construct a statistical model that separates fragile sites from regions showing signatures of positive selection for homozygous deletions and identify candidate tumour suppressors within those regions. We find 16 established tumour suppressors and propose 27 candidate tumour suppressors. Several of these genes (including MGMT, RAD17, and USP44) show prior evidence of a tumour suppressive function. Other candidate tumour suppressors, such as MAFTRR, KIAA1551, and IGF2BP2, are novel. Our study demonstrates how rare tumour suppressors can be identified through copy number meta-analysis. 1 Department of Electrical Engineering (ESAT) and iMinds Future Health Department, University of Leuven, Kasteelpark Arenberg 10, B-3001 Leuven, Belgium.
    [Show full text]
  • Valproic Acid Reversed Pathologic Endothelial Cell Gene Expression Profile Associated with Ischemia– Reperfusion Injury in a Swine Hemorrhagic Shock Model
    From the Peripheral Vascular Surgery Society Valproic acid reversed pathologic endothelial cell gene expression profile associated with ischemia– reperfusion injury in a swine hemorrhagic shock model Marlin Wayne Causey, MD,a Shashikumar Salgar, PhD,b Niten Singh, MD,a Matthew Martin, MD,a and Jonathan D. Stallings, PhD,b Tacoma, Wash Background: Vascular endothelial cells serve as the first line of defense for end organs after ischemia and reperfusion injuries. The full etiology of this dysfunction is poorly understood, and valproic acid (VPA) has proven to be beneficial after traumatic injury. The purpose of this study was to determine the mechanism of action through which VPA exerts its beneficial effects. Methods: Sixteen Yorkshire swine underwent a standardized protocol for an ischemia–reperfusion injury through received (6 ؍ hemorrhage and a supraceliac cross-clamp with ensuing 6-hour resuscitation. The experimental swine (n Aortic .(5 ؍ and injury-control models (n (5 ؍ VPA at cross-clamp application and were compared with sham (n endothelium was harvested, and microarray analysis was performed along with a functional clustering analysis with gene transcript validation using relative quantitative polymerase chain reaction. Results: Clinical comparison of experimental swine matched for sex, weight, and length demonstrated that VPA significantly decreased resuscitative requirements, with improved hemodynamics and physiologic laboratory measure- ments. Six transcript profiles from the VPA treatment were compared with the 1536 gene transcripts (529 up and 1007 down) from sham and injury-control swine. Microarray analysis and a Database for Annotation, Visualization and Integrated Discovery functional pathway analysis approach identified biologic processes associated with pathologic vascular endothelial function, specifically through functional cluster pathways involving apoptosis/cell death and angiogenesis/vascular development, with five specific genes (THBS1, TNFRSF12A, ANGPTL4, RHOB, and RTN4) identified as members of both functional clusters.
    [Show full text]
  • Supplementary Material Contents
    Supplementary Material Contents Immune modulating proteins identified from exosomal samples.....................................................................2 Figure S1: Overlap between exosomal and soluble proteomes.................................................................................... 4 Bacterial strains:..............................................................................................................................................4 Figure S2: Variability between subjects of effects of exosomes on BL21-lux growth.................................................... 5 Figure S3: Early effects of exosomes on growth of BL21 E. coli .................................................................................... 5 Figure S4: Exosomal Lysis............................................................................................................................................ 6 Figure S5: Effect of pH on exosomal action.................................................................................................................. 7 Figure S6: Effect of exosomes on growth of UPEC (pH = 6.5) suspended in exosome-depleted urine supernatant ....... 8 Effective exosomal concentration....................................................................................................................8 Figure S7: Sample constitution for luminometry experiments..................................................................................... 8 Figure S8: Determining effective concentration .........................................................................................................
    [Show full text]
  • A Software for Detection of Alternative Splicing Events in Human
    www.nature.com/scientificreports OPEN SpliceDetector: a software for detection of alternative splicing events in human and model Received: 21 June 2017 Accepted: 2 March 2018 organisms directly from transcript Published: xx xx xxxx IDs Mandana Baharlou Houreh1, Payam Ghorbani Kalkhajeh2, Ali Niazi1, Faezeh Ebrahimi3 & Esmaeil Ebrahimie 1,4,5,6 In eukaryotes, diferent combinations of exons lead to multiple transcripts with various functions in protein level, in a process called alternative splicing (AS). Unfolding the complexity of functional genomics through genome-wide profling of AS and determining the altered ultimate products provide new insights for better understanding of many biological processes, disease progress as well as drug development programs to target harmful splicing variants. The current available tools of alternative splicing work with raw data and include heavy computation. In particular, there is a shortcoming in tools to discover AS events directly from transcripts. Here, we developed a Windows-based user-friendly tool for identifying AS events from transcripts without the need to any advanced computer skill or database download. Meanwhile, due to online working mode, our application employs the updated SpliceGraphs without the need to any resource updating. First, SpliceGraph forms based on the frequency of active splice sites in pre-mRNA. Then, the presented approach compares query transcript exons to SpliceGraph exons. The tool provides the possibility of statistical analysis of AS events as well as AS visualization compared to SpliceGraph. The developed application works for transcript sets in human and model organisms. Transcripts are products of pre-mRNA splicing processes. Novel transcripts discover each day1,2 and add to public databases.
    [Show full text]
  • Identification of Genomic Targets of Krüppel-Like Factor 9 in Mouse Hippocampal
    Identification of Genomic Targets of Krüppel-like Factor 9 in Mouse Hippocampal Neurons: Evidence for a role in modulating peripheral circadian clocks by Joseph R. Knoedler A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Neuroscience) in the University of Michigan 2016 Doctoral Committee: Professor Robert J. Denver, Chair Professor Daniel Goldman Professor Diane Robins Professor Audrey Seasholtz Associate Professor Bing Ye ©Joseph R. Knoedler All Rights Reserved 2016 To my parents, who never once questioned my decision to become the other kind of doctor, And to Lucy, who has pushed me to be a better person from day one. ii Acknowledgements I have a huge number of people to thank for having made it to this point, so in no particular order: -I would like to thank my adviser, Dr. Robert J. Denver, for his guidance, encouragement, and patience over the last seven years; his mentorship has been indispensable for my growth as a scientist -I would also like to thank my committee members, Drs. Audrey Seasholtz, Dan Goldman, Diane Robins and Bing Ye, for their constructive feedback and their willingness to meet in a frequently cold, windowless room across campus from where they work -I am hugely indebted to Pia Bagamasbad and Yasuhiro Kyono for teaching me almost everything I know about molecular biology and bioinformatics, and to Arasakumar Subramani for his tireless work during the home stretch to my dissertation -I am grateful for the Neuroscience Program leadership and staff, in particular
    [Show full text]
  • The Pdx1 Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet Β Cell
    Page 1 of 125 Diabetes The Pdx1 bound Swi/Snf chromatin remodeling complex regulates pancreatic progenitor cell proliferation and mature islet β cell function Jason M. Spaeth1,2, Jin-Hua Liu1, Daniel Peters3, Min Guo1, Anna B. Osipovich1, Fardin Mohammadi3, Nilotpal Roy4, Anil Bhushan4, Mark A. Magnuson1, Matthias Hebrok4, Christopher V. E. Wright3, Roland Stein1,5 1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 2 Present address: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 3 Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 4 Diabetes Center, Department of Medicine, UCSF, San Francisco, California 5 Corresponding author: [email protected]; (615)322-7026 1 Diabetes Publish Ahead of Print, published online June 14, 2019 Diabetes Page 2 of 125 Abstract Transcription factors positively and/or negatively impact gene expression by recruiting coregulatory factors, which interact through protein-protein binding. Here we demonstrate that mouse pancreas size and islet β cell function are controlled by the ATP-dependent Swi/Snf chromatin remodeling coregulatory complex that physically associates with Pdx1, a diabetes- linked transcription factor essential to pancreatic morphogenesis and adult islet-cell function and maintenance. Early embryonic deletion of just the Swi/Snf Brg1 ATPase subunit reduced multipotent pancreatic progenitor cell proliferation and resulted in pancreas hypoplasia. In contrast, removal of both Swi/Snf ATPase subunits, Brg1 and Brm, was necessary to compromise adult islet β cell activity, which included whole animal glucose intolerance, hyperglycemia and impaired insulin secretion. Notably, lineage-tracing analysis revealed Swi/Snf-deficient β cells lost the ability to produce the mRNAs for insulin and other key metabolic genes without effecting the expression of many essential islet-enriched transcription factors.
    [Show full text]
  • Fusion Genes in Gynecologic Tumors: the Occurrence, Molecular Mechanism and Prospect for Therapy ✉ Bingfeng Lu1, Ruqi Jiang1, Bumin Xie1,Wuwu1 and Yang Zhao 1
    www.nature.com/cddis REVIEW ARTICLE OPEN Fusion genes in gynecologic tumors: the occurrence, molecular mechanism and prospect for therapy ✉ Bingfeng Lu1, Ruqi Jiang1, Bumin Xie1,WuWu1 and Yang Zhao 1 © The Author(s) 2021 Gene fusions are thought to be driver mutations in multiple cancers and are an important factor for poor patient prognosis. Most of them appear in specific cancers, thus satisfactory strategies can be developed for the precise treatment of these types of cancer. Currently, there are few targeted drugs to treat gynecologic tumors, and patients with gynecologic cancer often have a poor prognosis because of tumor progression or recurrence. With the application of massively parallel sequencing, a large number of fusion genes have been discovered in gynecologic tumors, and some fusions have been confirmed to be involved in the biological process of tumor progression. To this end, the present article reviews the current research status of all confirmed fusion genes in gynecologic tumors, including their rearrangement mechanism and frequency in ovarian cancer, endometrial cancer, endometrial stromal sarcoma, and other types of uterine tumors. We also describe the mechanisms by which fusion genes are generated and their oncogenic mechanism. Finally, we discuss the prospect of fusion genes as therapeutic targets in gynecologic tumors. Cell Death and Disease (2021) 12:783 ; https://doi.org/10.1038/s41419-021-04065-0 FACTS Generally, at the genome level, the fusion gene may be expressed; however, if the promoter region or other important elements are destroyed, it may not be expressed. In 1973, researchers first ● fi Fusion genes are cancer-speci c and considered to be the discovered the rearrangement of chromosomes 9 and 22 in driving events of cancer.
    [Show full text]