Mouse Tmem106a Knockout Project (CRISPR/Cas9)
Total Page：16
File Type：pdf, Size：1020Kb
Load more
Recommended publications
-
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. -
TMEM106B in Humans and Vac7 and Tag1 in Yeast Are Predicted to Be Lipid Transfer Proteins
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.12.435176; this version posted March 12, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. TMEM106B in humans and Vac7 and Tag1 in yeast are predicted to be lipid transfer proteins Tim P. Levine* UCL Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, United Kingdom. ORCID 0000-0002-7231-0775 *Corresponding author and lead contact: [email protected] Data availability statement: The data that support this study are freely available in Harvard Dataverse at https://dataverse.harvard.edu/dataverse/LEA_2. Acknowledgements: work was funded by the Higher Education Funding Council for England and the NIHR Moorfields Biomedical Research Centre Conflict of interest disclosure: the author declares that there is no conflict of interest Keywords: Structural bioinformatics, Lipid transfer protein, LEA_2, TMEM106B, Vac7, YLR173W, Endosome, Lysosome Running Title: TMEM106B & Vac7: lipid transfer proteins 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.12.435176; this version posted March 12, 2021. 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 TMEM106B is an integral membrane protein of late endosomes and lysosomes involved in neuronal function, its over-expression being associated with familial frontotemporal lobar degeneration, and under-expression linked to hypomyelination. It has also been identified in multiple screens for host proteins required for productive SARS-CoV2 infection. Because standard approaches to understand TMEM106B at the sequence level find no homology to other proteins, it has remained a protein of unknown function. -
Association Weight Matrix for the Genetic Dissection of Puberty in Beef Cattle
Association weight matrix for the genetic dissection of puberty in beef cattle Marina R. S. Fortesa,b,c, Antonio Revertera,b, Yuandan Zhanga,d, Eliza Collisa,b, Shivashankar H. Nagarajb,NickN.Jonssona,c,e, Kishore C. Prayagaa,b,1, Wes Barrisa,b, and Rachel J. Hawkena,b,2 aCooperative Research Centre for Beef Genetic Technologies; bCommonwealth Scientific and Industrial Research Organization, division of Livestock Industries, Queensland Bioscience Precinct, Brisbane QLD 4067, Australia; cThe University of Queensland, School of Veterinary Science, Gatton QLD 4343, Australia; dAnimal Genetics and Breeding Unit, University of New England, Armidale NSW 2351, Australia; and eFaculty of Veterinary Medicine, University of Glasgow, Glasgow G61 1QH, United Kingdom Edited by George Seidel, Colorado State University, Fort Collins, CO, and approved June 21, 2010 (received for review February 23, 2010) We describe a systems biology approach for the genetic dissection tional data on traits related to puberty are available. For example, of complex traits based on applying gene network theory to the re- weight and condition score are often measured on occasions sults from genome-wide associations. The associations of single- throughout an animal’s development. Hence, understanding ge- nucleotide polymorphisms (SNP) that were individually associated netics of cattle puberty and its biology serves two purposes: as with a primary phenotype of interest, age at puberty in our study, a strategy to develop efficient livestock resources and as a model were explored across 22 related traits. Genomic regions were sur- for human biology. veyed for genes harboring the selected SNP. As a result, an asso- The focus of this work is to demonstrate a unique systems ap- ciation weight matrix (AWM) was constructed with as many rows proach, which we call an association weight matrix (AWM), ap- as genes and as many columns as traits. -
NBR1 (D2E6) Rabbit Mab A
Revision 1 C 0 2 - t NBR1 (D2E6) Rabbit mAb a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 1 9 Web: [email protected] 8 www.cellsignal.com 9 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source/Isotype: UniProt ID: Entrez-Gene Id: WB, IP, IF-IC, F H M Endogenous 120 Rabbit IgG Q14596 4077 Product Usage Information Application Dilution Western Blotting 1:1000 Immunoprecipitation 1:50 Immunofluorescence (Immunocytochemistry) 1:1600 Flow Cytometry 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody. Specificity / Sensitivity NBR1 (D2E6) Rabbit mAb recognizes endogenous levels of total NBR1 protein. Species Reactivity: Human, Mouse Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys601 of human NBR1 protein. Background Next to BRCA1 gene 1 (NBR1) protein is known for its encoding gene proximity to the BRCA1 tumor suppressor gene (1,2). N-terminal Phox and Bem1p (PB1) domains of NBR1 mediate its interaction with muscle specific titin kinase (3,4) and scaffolding protein p62 (4). NBR1 plays a role in autophagy by facilitating the autophagosomal degradation of ubiquitinated proteins independently and also in concert with p62 (5,6). 1. Campbell, I.G. et al. (1994) Hum Mol Genet 3, 589-94. 2. -
Anti-TMEM106A (RABBIT) Antibody - 600-401-FH1
Anti-TMEM106A (RABBIT) Antibody - 600-401-FH1 Code: 600-401-FH1 Size: 100 µg Product Description: Anti-TMEM106A (RABBIT) Antibody - 600-401-FH1 Concentration: 1 mg/mL by UV absorbance at 280 nm PhysicalState: Liquid (sterile filtered) Label Unconjugated Host Rabbit Gene Name TMEM106A Species Reactivity Human, mouse Buffer 0.01 M Sodium Phosphate, 0.25 M Sodium Chloride, pH 7.2 Stabilizer None Preservative 0.02% (w/v) Sodium Azide Storage Condition Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use. Synonyms TMEM106A Antibody, Transmembrane protein 106A Application Note Anti-TMEM106A Antibody has been tested for use in ELISA, Western Blotting, Immunohistochemistry and Immunofluorescence. Specific conditions for reactivity should be optimized by the end user. Expect a band at approximately 29 kDa in Western Blots of specific cell lysates and tissues. Background Transmembrane protein 106A (TMEM106A) is a single-pass transmembrane protein that is closely related to TMEM106B, a protein that is thought to be a novel risk factor for frontotemporal lobar degeneration (FTLD), a group of clinically, pathologically and genetically heterogeneous disorders associated with atrophy in the frontal lobe and temporal lobe of the brain. The actual roles of TMEM106A and TMEM106B are still undetermined; however, as TMEM106B is involved in FTLD, it is possible that TMEM106A may also be a risk factor for FTLD. -
Increased Expression of the Frontotemporal Dementia Risk Factor Tmem106b Causes C9orf72-Dependent Alterations in Lysosomes
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2016 Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways Johanna Irene Busch University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Cell Biology Commons, and the Neuroscience and Neurobiology Commons Recommended Citation Busch, Johanna Irene, "Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways" (2016). Publicly Accessible Penn Dissertations. 1630. https://repository.upenn.edu/edissertations/1630 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1630 For more information, please contact [email protected]. Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways Abstract Frontotemporal lobar degeneration (FTLD) is an important cause of dementia in individuals under age 65. Common variants in the TMEM106B gene were previously discovered by genome-wide association (GWAS) to confer genetic risk for FTLD-TDP, the largest neuropathological subset of FTLD (p=1x10-11, OR=1.6). Prior to its discovery in the GWAS, TMEM106B, or Transmembrane Protein 106B, was uncharacterized. To further understand the role of TMEM106B in disease pathogenesis, we used immortalized as well as primary neurons to assess the cell biological effects of disease-relevant levels of TMEM106B overexpression and the interaction of TMEM106B with additional disease-associated proteins. We also employed immunostaining to assess its expression pattern in human brain from controls and FTLD cases. We discovered that TMEM106B is a highly glycosylated, Type II late endosomal/lysosomal transmembrane protein. We found that it is expressed by neurons, glia, and peri-vascular cells in disease- affected and unaffected regions of human brain from normal controls in a cytoplasmic, perikaryal distribution. -
Datasheet: MCA3240Z Product Details
Datasheet: MCA3240Z Description: MOUSE ANTI HUMAN NBR1:Preservative Free Specificity: NBR1 Format: Preservative Free Product Type: Monoclonal Antibody Clone: 6B11 Isotype: IgG1 Quantity: 0.1 mg Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio-rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Western Blotting 0.1 - 10 ug/ml Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Target Species Human Product Form Purified IgG - liquid Preparation Purified IgG prepared by affinity chromatography on Protein A Buffer Solution Phosphate buffered saline Preservative None present Stabilisers Approx. Protein Ig concentration 0.5 mg/ml Concentrations Immunogen Recombinant protein corresponding to aa 2-97 of human NBR1 External Database Links UniProt: Q14596 Related reagents Entrez Gene: 4077 NBR1 Related reagents Synonyms 1A13B, KIAA0049, M17S2 Page 1 of 3 Fusion Partners Spleen cells from BALB/c mice were fused with cells from the Sp2/0 myeloma cell line. Specificity Mouse anti Human NBR1 antibody, clone 6B11 recognizes human Next to BRCA1 gene 1 protein, also known as NBR1, Cell migration-inducing gene 19 protein, Membrane component chromosome 17 surface marker 2, Neighbor of BRCA1 gene 1 protein or Protein 1A1-3B. -
SUPPLEMENTARY MATERIAL Supplementary Fig. S1. LD Mice Used in This Study Accumulate Polyglucosan Inclusions (Lafora Bodies) in the Brain
1 SUPPLEMENTARY MATERIAL Supplementary Fig. S1. LD mice used in this study accumulate polyglucosan inclusions (Lafora bodies) in the brain. Samples from the hippocampus of five months old control, Epm2a-/- (lacking laforin) and Epm2b-/- mice (lacking malin) were stained with periodic acid Schiff reagent (PAS staining), which colors polysaccharide granules in red. Bar: 50 m. Supplementary Fig. S2. Principal component analysis (PCA) representing the first two components with the biggest level of phenotypic variability. Samples 1_S1 to 4_S4 corresponded to control, 5_S5, 6_S6 and 8_S8 to Epm2a-/- and 9_S9 to 12_S12 to Epm2b- /- samples, of animals of 16 months of age respectively. Supplementary Table S1. Primers used in this work to validate the expression of the corresponding genes by RT-qPCR. Supplementary Table S2: Genes downregulated more than 0.5 fold in Epm2a-/- and Epm2b-/- mice of 16 months of age. The gene name, false discovery rate (FDR), fold change (FC), description and MGI Id (mouse genome informatics) are indicated. Genes are arranged according to FC. Supplementary Table S3: Genes upregulated more than 1.5 fold in Epm2a-/- mice of 16 months of age. The gene name, false discovery rate (FDR), fold change (FC), description and MGI Id (mouse genome informatics) are indicated. Genes are arranged according to FC. Supplementary Table S4: Genes upregulated more than 1.5 fold in Epm2b-/- mice of 16 months of age. The gene name, false discovery rate (FDR), fold change (FC), description and MGI Id (mouse genome informatics) are indicated. Genes are arranged according to FC. 2 Supplementary Table S5: Genes upregulated in both Epm2a-/- and Epm2b-/- mice of 16 months of age. -
Transmembrane Protein 106A Activates Mouse Peritoneal Macrophages Via the MAPK and NF-Κb Signaling Pathways
www.nature.com/scientificreports OPEN Transmembrane protein 106a activates mouse peritoneal macrophages via the MAPK and Received: 06 January 2015 Accepted: 30 June 2015 NF-κB signaling pathways Published: 28 July 2015 Hui Dai1, Dong Xu1,2, Jing Su3, Jingyuan Jang1 & Yingyu Chen1,2 The M1 and M2 states of macrophage are the two extremes of a physiologic/phenotypic continuum that is dynamically influenced by environmental signals. Molecular mechanism analysis indicated that they gain M1 and M2-related functions after encountering specific ligands in the tissue environment. Here, we first characterized the previously unknown immunobiological functions of mouse Tmem106a. This protein is abundantly expressed on the surface of mouse macrophages. Activation of Tmem106a by stimulation with anti-Tmem106a upregulated the expression of CD80, CD86, CD69 and MHC II on macrophage, and induced the release of TNF-α, IL-1β, IL-6, CCL2 and NO, but not IL-10. These effects were largely abrogated by pretreatment with siRNA against Tmem106a. Notably, anti-Tmem106a significantly increased iNOS production and phosphorylation of STAT1, and had no effect on the ARGINASE-1 or p-STAT6 level, indicating that anti-Tmem106a activated macrophages and polarized them into M1-like macrophages. Further analysis found that anti-Tmem106a stimulation increased phosphorylation of ERK-1/2, JNK, p38 MAPK, NF-κB p65 and IKKα/β, and promoted nuclear translocation of the cytosolic NF-κB p65 subunit. Collectively, these data suggest that mouse Tmem106a might be a new trigger of macrophage activation and have some influence toward the M1 state through the activation of the MAPKs and NF-κB pathway. -
(12) Patent Application Publication (10) Pub. No.: US 2013/0130246A1 BENSMON Et Al
US 2013 O130246A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0130246A1 BENSMON et al. (43) Pub. Date: May 23, 2013 (54) METHODS FOR THE DETECTION, (22) Filed: Oct. 31, 2012 VISUALIZATION AND HIGH RESOLUTION PHYSICAL MAPPING OF GENOMIC Related U.S. Application Data REARRANGEMENTS IN BREAST AND OVARAN CANCER GENES AND LOC (60) Provisional application No. 61/553,906, filed on Oct. BRCA1 AND BRCA2 USING GENOMIC 31, 2011. MORSE CODE IN CONJUNCTION WITH MOLECULAR COMBING Publication Classification (71) Applicants: Aaron BENSIMON, Anthony (FR): (51) Int. Cl. Maurizio Ceppi, Issy-Les-Moulineaux CI2O I/68 (2006.01) (FR); Kevin Cheeseman, (52) U.S. Cl. Champigny-Sur-Marne (FR); Emmanuel CPC .................................... CI2O I/6886 (2013.01) Conseiller, Paris (FR); Pierre Walrafen, USPC ......................................................... 435/6.11 Montrouge (FR) (57) ABSTRACT (72) Inventors: Aaron BENSIMON, Anthony (FR): Maurizio Ceppi, Issy-Les-Moulineaux Methods for detecting genomic rearrangements in BRCA1 (FR); Kevin Cheeseman, and BRCA2 genes at high resolution using Molecular Comb Champigny-Sur-Marne (FR); Emmanuel ing and for determining a predisposition to a disease or dis Conseiller, Paris (FR); Pierre Walrafen, order associated with these rearrangements including predis Montrouge (FR) position to ovarian cancer or breast cancer. Primers useful for producing probes for this method and kits for practicing the (21) Appl. No.: 13/665,404 methods. Patent Application Publication May 23, 2013 Sheet 1 of 12 US 2013/0130246 A1 85925 379 o : 98. xxxxxx& 3850,75800 :g i s Patent Application Publication May 23, 2013 Sheet 2 of 12 US 2013/0130246 A1 Fig. 1B 845 3.25° 42950 888 O 3690 73800 O700 147600' S. -
NBR1 Sirna (H): Sc-94187
SANTA CRUZ BIOTECHNOLOGY, INC. NBR1 siRNA (h): sc-94187 BACKGROUND SUPPORT REAGENTS NBR1 (neighbor of BRCA1 gene 1), also known as M17S2, MIG19 or 1A13B, is For optimal siRNA transfection efficiency, Santa Cruz Biotechnology’s a 966 amino acid protein that is encoded by a gene neighboring the well-char- siRNA Transfection Reagent: sc-29528 (0.3 ml), siRNA Transfection Medium: acterized tumor suppressor BRCA1. Originally thought to be the ovarian cancer sc-36868 (20 ml) and siRNA Dilution Buffer: sc-29527 (1.5 ml) are recom- antigen CA125, NBR1 contains structural motifs, including a B-box/coiled coil mended. Control siRNAs or Fluorescein Conjugated Control siRNAs are domain, an OPR domain and a ZZ-type zinc finger, that are characteristic of available as 10 µM in 66 µl. Each contain a scrambled sequence that will several proteins involved in cell transformation. NBR1 interacts with SQSTM1 not lead to the specific degradation of any known cellular mRNA. Fluorescein (sequestosome 1 protein), Titin and MuRF2 (muscle-specific RING finger pro- Conjugated Control siRNAs include: sc-36869, sc-44239, sc-44240 and tein 2), suggesting a possible role in developmental pathways. Two isoforms, sc-44241. Control siRNAs include: sc-37007, sc-44230, sc-44231, sc-44232, designated NBR1A and NBR1B, are expressed due to alternative splicing sc-44233, sc-44234, sc-44235, sc-44236, sc-44237 and sc-44238. events. Expression of both isoforms is downregulated in malignant mammary tissues, indicating that NBR1 may be involved in tumor suppression. GENE EXPRESSION MONITORING NBR1 (4BR): sc-130380 is recommended as a control antibody for monitoring REFERENCES of NBR1 gene expression knockdown by Western Blotting (starting dilution 1. -
Identification and Comprehensive Characterization of Large Genomic
Identification and comprehensive characterization of large genomic rearrangements in the and genes Jesús Valle, Lídia Feliubadaló, Marga Nadal, Alex Teulé, Rosa Miró, Raquel Cuesta, Eva Tornero, Mireia Menéndez, Esther Darder, Joan Brunet, et al. To cite this version: Jesús Valle, Lídia Feliubadaló, Marga Nadal, Alex Teulé, Rosa Miró, et al.. Identification and com- prehensive characterization of large genomic rearrangements in the and genes. Breast Cancer Re- search and Treatment, Springer Verlag, 2009, 122 (3), pp.733-743. 10.1007/s10549-009-0613-9. hal- 00535410 HAL Id: hal-00535410 https://hal.archives-ouvertes.fr/hal-00535410 Submitted on 11 Nov 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Breast Cancer Res Treat (2010) 122:733–743 DOI 10.1007/s10549-009-0613-9 PRECLINICAL STUDY Identification and comprehensive characterization of large genomic rearrangements in the BRCA1 and BRCA2 genes Jesu´s del Valle • Lı´dia Feliubadalo´ • Marga Nadal • Alex Teule´ • Rosa Miro´ • Raquel Cuesta • Eva Tornero • Mireia Mene´ndez • Esther Darder • Joan Brunet • Gabriel Capella` • Ignacio Blanco • Conxi La´zaro Received: 26 August 2009 / Accepted: 20 October 2009 / Published online: 6 November 2009 Ó Springer Science+Business Media, LLC.