KT33B Polyclonal Antibody Product Information

Total Page：16

File Type：pdf, Size：1020Kb

KT33B Polyclonal Antibody Product Information

KT33B Polyclonal Antibody Cat #: ABP59086 Size: 30μl /100μl /200μl Product Information Product Name: KT33B Polyclonal Antibody Applications: WB, ELISA Isotype: Rabbit IgG Reactivity: Human Catalog Number: ABP59086 Lot Number: Refer to product label Formulation: Liquid Concentration: 1 mg/ml Storage: Store at -20°C. Avoid repeated Note: Contain sodium azide. freeze / thaw cycles. Background: KRT33B (Keratin 33B) is a Protein Coding gene. Among its related pathways are Keratinization and Developmental Biology. KRT33B encodes a member of the keratin gene family. KRT33B is one of multiple type I hair keratin genes that are clustered in a region of chromosome 17q12-q21 and have the same direction of transcription. As a type I hair keratin, the encoded protein is an acidic protein which heterodimerizes with type II keratins to form hair and nails. There are two isoforms of this protein, encoded by two separate genes, keratin 33A and keratin 33B. Application Notes: Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB (1:500-1:2000), ELISA (1:5000-1:20000). Storage Buffer: PBS, pH 7.4, containing 0.02% Sodium Azide as preservative and 50% Glycerol. Storage Instructions: Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing. Note: The product listed herein is for research use only and is not intended for use in human or clinical diagnosis. Suggested applications of our products are not recommendations to use our products in violation of any patent or as a license. We cannot be responsible for patent infringements or other violations that may occur with the use of this product. Version 201805 Abbkine, Inc • China • www.abbkine.com Not for further distribution without written consent.Copyright © Abbkine, Inc..

Copy Link

Recommended publications

FK506-Binding Protein 12.6/1B, a Negative Regulator of [Ca2+], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. A link to any extended data will be provided when the final version is posted online. Research Articles: Neurobiology of Disease FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats John C. Gant1, Eric M. Blalock1, Kuey-Chu Chen1, Inga Kadish2, Olivier Thibault1, Nada M. Porter1 and Philip W. Landfield1 1Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536 2Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294 DOI: 10.1523/JNEUROSCI.2234-17.2017 Received: 7 August 2017 Revised: 10 October 2017 Accepted: 24 November 2017 Published: 18 December 2017 Author contributions: J.C.G. and P.W.L. designed research; J.C.G., E.M.B., K.-c.C., and I.K. performed research; J.C.G., E.M.B., K.-c.C., I.K., and P.W.L. analyzed data; J.C.G., E.M.B., O.T., N.M.P., and P.W.L. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. NIH grants AG004542, AG033649, AG052050, AG037868 and McAlpine Foundation for Neuroscience Research Corresponding author: Philip W. Landfield, [email protected], Department of Pharmacology & Nutritional Sciences, University of Kentucky, 800 Rose Street, UKMC MS 307, Lexington, KY 40536 Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2234-17.2017 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published.
[Show full text]
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.
[Show full text]
The Correlation of Keratin Expression with In-Vitro Epithelial Cell Line Differentiation
The correlation of keratin expression with in-vitro epithelial cell line differentiation Deeqo Aden Thesis submitted to the University of London for Degree of Master of Philosophy (MPhil) Supervisors: Professor Ian. C. Mackenzie Professor Farida Fortune Centre for Clinical and Diagnostic Oral Science Barts and The London School of Medicine and Dentistry Queen Mary, University of London 2009 Contents Content pages ……………………………………………………………………......2 Abstract………………………………………………………………………….........6 Acknowledgements and Declaration……………………………………………...…7 List of Figures…………………………………………………………………………8 List of Tables………………………………………………………………………...12 Abbreviations….………………………………………………………………..…...14 Chapter 1: Literature review 16 1.1 Structure and function of the Oral Mucosa……………..…………….…..............17 1.2 Maintenance of the oral cavity...……………………………………….................20 1.2.1 Environmental Factors which damage the Oral Mucosa………. ….…………..21 1.3 Structure and function of the Oral Mucosa ………………...….……….………...21 1.3.1 Skin Barrier Formation………………………………………………….……...22 1.4 Comparison of Oral Mucosa and Skin…………………………………….……...24 1.5 Developmental and Experimental Models used in Oral mucosa and Skin...……..28 1.6 Keratinocytes…………………………………………………….….....................29 1.6.1 Desmosomes…………………………………………….…...............................29 1.6.2 Hemidesmosomes……………………………………….…...............................30 1.6.3 Tight Junctions………………………….……………….…...............................32 1.6.4 Gap Junctions………………………….……………….….................................32
[Show full text]
MALE Protein Name Accession Number Molecular Weight CP1 CP2 H1 H2 PDAC1 PDAC2 CP Mean H Mean PDAC Mean T-Test PDAC Vs. H T-Test
MALE t-test t-test Accession Molecular H PDAC PDAC vs. PDAC vs. Protein Name Number Weight CP1 CP2 H1 H2 PDAC1 PDAC2 CP Mean Mean Mean H CP PDAC/H PDAC/CP - 22 kDa protein IPI00219910 22 kDa 7 5 4 8 1 0 6 6 1 0.1126 0.0456 0.1 0.1 - Cold agglutinin FS-1 L-chain (Fragment) IPI00827773 12 kDa 32 39 34 26 53 57 36 30 55 0.0309 0.0388 1.8 1.5 - HRV Fab 027-VL (Fragment) IPI00827643 12 kDa 4 6 0 0 0 0 5 0 0 - 0.0574 - 0.0 - REV25-2 (Fragment) IPI00816794 15 kDa 8 12 5 7 8 9 10 6 8 0.2225 0.3844 1.3 0.8 A1BG Alpha-1B-glycoprotein precursor IPI00022895 54 kDa 115 109 106 112 111 100 112 109 105 0.6497 0.4138 1.0 0.9 A2M Alpha-2-macroglobulin precursor IPI00478003 163 kDa 62 63 86 72 14 18 63 79 16 0.0120 0.0019 0.2 0.3 ABCB1 Multidrug resistance protein 1 IPI00027481 141 kDa 41 46 23 26 52 64 43 25 58 0.0355 0.1660 2.4 1.3 ABHD14B Isoform 1 of Abhydrolase domain-containing proteinIPI00063827 14B 22 kDa 19 15 19 17 15 9 17 18 12 0.2502 0.3306 0.7 0.7 ABP1 Isoform 1 of Amiloride-sensitive amine oxidase [copper-containing]IPI00020982 precursor85 kDa 1 5 8 8 0 0 3 8 0 0.0001 0.2445 0.0 0.0 ACAN aggrecan isoform 2 precursor IPI00027377 250 kDa 38 30 17 28 34 24 34 22 29 0.4877 0.5109 1.3 0.8 ACE Isoform Somatic-1 of Angiotensin-converting enzyme, somaticIPI00437751 isoform precursor150 kDa 48 34 67 56 28 38 41 61 33 0.0600 0.4301 0.5 0.8 ACE2 Isoform 1 of Angiotensin-converting enzyme 2 precursorIPI00465187 92 kDa 11 16 20 30 4 5 13 25 5 0.0557 0.0847 0.2 0.4 ACO1 Cytoplasmic aconitate hydratase IPI00008485 98 kDa 2 2 0 0 0 0 2 0 0 - 0.0081 - 0.0
[Show full text]
Downloaded 18 July 2014 with a 1% False Discovery Rate (FDR)
UC Berkeley UC Berkeley Electronic Theses and Dissertations Title Chemical glycoproteomics for identification and discovery of glycoprotein alterations in human cancer Permalink https://escholarship.org/uc/item/0t47b9ws Author Spiciarich, David Publication Date 2017 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California Chemical glycoproteomics for identification and discovery of glycoprotein alterations in human cancer by David Spiciarich A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Chemistry in the Graduate Division of the University of California, Berkeley Committee in charge: Professor Carolyn R. Bertozzi, Co-Chair Professor David E. Wemmer, Co-Chair Professor Matthew B. Francis Professor Amy E. Herr Fall 2017 Chemical glycoproteomics for identification and discovery of glycoprotein alterations in human cancer © 2017 by David Spiciarich Abstract Chemical glycoproteomics for identification and discovery of glycoprotein alterations in human cancer by David Spiciarich Doctor of Philosophy in Chemistry University of California, Berkeley Professor Carolyn R. Bertozzi, Co-Chair Professor David E. Wemmer, Co-Chair Changes in glycosylation have long been appreciated to be part of the cancer phenotype; sialylated glycans are found at elevated levels on many types of cancer and have been implicated in disease progression. However, the specific glycoproteins that contribute to cell surface sialylation are not well characterized, specifically in bona fide human cancer. Metabolic and bioorthogonal labeling methods have previously enabled enrichment and identification of sialoglycoproteins from cultured cells and model organisms. The goal of this work was to develop technologies that can be used for detecting changes in glycoproteins in clinical models of human cancer.
[Show full text]
Transcriptome Profiling and Differential Gene Expression In
G C A T T A C G G C A T genes Article Transcriptome Profiling and Differential Gene Expression in Canine Microdissected Anagen and Telogen Hair Follicles and Interfollicular Epidermis Dominique J. Wiener 1,* ,Kátia R. Groch 1 , Magdalena A.T. Brunner 2,3, Tosso Leeb 2,3 , Vidhya Jagannathan 2 and Monika M. Welle 3,4 1 Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Science, Texas A&M University, College Station, TX 77843, USA; [email protected] 2 Institute of Genetics, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland; [email protected] (M.A.T.B.); [email protected] (T.L.); [email protected] (V.J.) 3 Dermfocus, Vetsuisse Faculty, University Hospital of Bern, 3010 Bern, Switzerland; [email protected] 4 Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland * Correspondence: [email protected]; Tel.: +1-979-862-1568 Received: 30 June 2020; Accepted: 3 August 2020; Published: 4 August 2020 Abstract: The transcriptome profile and differential gene expression in telogen and late anagen microdissected hair follicles and the interfollicular epidermis of healthy dogs was investigated by using RNAseq. The genes with the highest expression levels in each group were identified and genes known from studies in other species to be associated with structure and function of hair follicles and epidermis were evaluated. Transcriptome profiling revealed that late anagen follicles expressed mainly keratins and telogen follicles expressed GSN and KRT15. The interfollicular epidermis expressed predominately genes encoding for proteins associated with differentiation. All sample groups express genes encoding for proteins involved in cellular growth and signal transduction.
[Show full text]
Effect of Selenocystine on Gene Expression Profiles in Human Keloid
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Genomics 97 (2011) 265–276 Contents lists available at ScienceDirect Genomics journal homepage: www.elsevier.com/locate/ygeno Effect of selenocystine on gene expression profiles in human keloid fibroblasts Bruna De Felice a,⁎, Corrado Garbi b, Robert R. Wilson a, Margherita Santoriello b, Massimo Nacca a a Department of Life Sciences, University of Naples II, Via Vivaldi 43, 81100 Caserta, Italy b Department of Cellular and Molecular Biology and Pathology, University of Naples “Federico II”, Naples, Italy article info abstract Article history: In this study, selenocystine, a nutritionally available selenoamino acid, was identified for the first time as a Received 15 October 2010 novel agent with anti proliferative activity on human keloids. Accepted 24 February 2011 The 20 μM concentration after 48 h treatment used here was the most effective to reduce keloid fibroblast Available online 1 March 2011 growth. We analyzed the gene expression profile of selenocystine treatment response in keloid fibroblasts by the microarray system to characterize the effects of selenocystine on human keloids. Keywords: The major alterations in keloid fibroblasts following selenocystine exposure included up-regulation of the Keloids Microarray genes encoding cell death and transcription factors. Prominent down-regulation of genes involved in Selenocystine development, cell adhesion and cytoskeleton, as well as extra cellular matrix genes, usually strongly up- Gene expression regulated in keloids, resulted following selenocystine exposure. The range of the down-regulated genes and the degree of the decreased expression appeared to be correlated with the degree of the morphological alterations in selenocystine treated keloids.
[Show full text]
Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham a Thesis Submitted in Conformity
Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Molecular Genetics University of Toronto © Copyright by Edward James Higginbotham 2020 i Abstract Characterizing Genomic Duplication in Autism Spectrum Disorder Edward James Higginbotham Master of Science Graduate Department of Molecular Genetics University of Toronto 2020 Duplication, the gain of additional copies of genomic material relative to its ancestral diploid state is yet to achieve full appreciation for its role in human traits and disease. Challenges include accurately genotyping, annotating, and characterizing the properties of duplications, and resolving duplication mechanisms. Whole genome sequencing, in principle, should enable accurate detection of duplications in a single experiment. This thesis makes use of the technology to catalogue disease relevant duplications in the genomes of 2,739 individuals with Autism Spectrum Disorder (ASD) who enrolled in the Autism Speaks MSSNG Project. Fine-mapping the breakpoint junctions of 259 ASD-relevant duplications identified 34 (13.1%) variants with complex genomic structures as well as tandem (193/259, 74.5%) and NAHR- mediated (6/259, 2.3%) duplications. As whole genome sequencing-based studies expand in scale and reach, a continued focus on generating high-quality, standardized duplication data will be prerequisite to addressing their associated biological mechanisms. ii Acknowledgements I thank Dr. Stephen Scherer for his leadership par excellence, his generosity, and for giving me a chance. I am grateful for his investment and the opportunities afforded me, from which I have learned and benefited. I would next thank Drs.
[Show full text]
Mouse Krt33b Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Krt33b Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Krt33b conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Krt33b gene (NCBI Reference Sequence: NM_013570 ; Ensembl: ENSMUSG00000057723 ) is located on Mouse chromosome 11. 7 exons are identified, with the ATG start codon in exon 1 and the TAA stop codon in exon 7 (Transcript: ENSMUST00000073890). Exon 3 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Krt33b gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-351F1 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 3 starts from about 35.64% of the coding region. The knockout of Exon 3 will result in frameshift of the gene. The size of intron 2 for 5'-loxP site insertion: 879 bp, and the size of intron 3 for 3'-loxP site insertion: 795 bp. The size of effective cKO region: ~657 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele gRNA region 5' gRNA region 3' 1 2 3 4 5 6 7 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Krt33b Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats.
[Show full text]
Genetic and Functional Investigation of Inherited Neuropathies
GENETIC AND FUNCTIONAL INVESTIGATION OF INHERITED NEUROPATHIES Ellen Cottenie MRC Centre for Neuromuscular Diseases, UCL Institute of Neurology Supervisors: Professor Mary M. Reilly, Professor Henry Houlden and Professor Mike Hanna Thesis submitted for the degree of Doctor of Philosophy University College London 2015 1 Declaration I, Ellen Cottenie, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. 2 Abstract With the discovery of next generation sequencing techniques the landscape of pathogenic gene discovery has shifted drastically over the last ten years. For the purpose of this thesis, focus was applied on finding genetic causes of inherited neuropathies, mainly Charcot-Marie-Tooth disease, by using both old and new genetic techniques and the accompanying functional investigations to prove the pathogenicity of these variants. Mutations in ATPase 6, the first mitochondrially encoded gene responsible for an isolated neuropathy, were found in five families with CMT2 by a traditional Sanger sequencing approach. The same approach was used to expand the phenotype associated with FIG4 mutations, known as CMT4J. Compound heterozygous mutations were found in a patient with a proximal and asymmetric weakness and rapid deterioration of strength in a single limb, mimicking CIDP. Several appropriate cohorts were screened for mutations in candidate genes with the traditional Sanger sequencing approach; however, no new pathogenic genes were found. In the case of the HINT1 gene, the originally stated frequency of 11% could not be replicated and a founder effect was suggested, underlying the importance of considering the ethnic background of a patient when screening for mutations in neuropathy-related genes.
[Show full text]
Keratin-Mediated Hair Growth
Keratin is not only a Structural Protein in Hair: Keratin-mediated Hair Growth Seong Yeong An Kyung Hee University Eun Ji Choi Konkuk University So Yeon Kim Kyung Hee University Se Young Van Kyung Hee University Han Jun Kim Konkuk University Jae-Hyung Lee Kyung Hee University https://orcid.org/0000-0002-5085-6988 Song Wook Han KeraMedix Inc Il Keun Kwon Kyung Hee University Chul-Kyu Lee Chemon Inc. Sun Hee Do Konkuk University Yu-Shik Hwang ( [email protected] ) Kyung Hee University Article Keywords: Keratin , hair, intradermal injection, outer root sheath cells, Posted Date: November 18th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-101358/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/27 Abstract Keratin is known to be a major protein in hair, but the biological function of keratin in hair growth is unknown, which led us to conduct a pilot study to elucidate biological function of keratin in hair growth via cellular interactions with hair forming cells. Here, we show hair growth is stimulated by intradermal injection of keratin into mice, and show that outer root sheath cells undergo transforming growth factor- β2-induced apoptosis, resulting in keratin exposure. Keratin exposure appears to be critical for dermal papilla cell condensation and hair germ formation as immunodepletion and silencing keratin prevent dermal papilla cell condensation and hair germ formation. Furthermore, silencing keratin in mice resulted in a marked suppression of anagen follicle formation and hair growth. Our study imply a new nding of how to initiate hair regeneration and suggests the potent application of keratin biomaterial for the treatment of hair loss.
[Show full text]
(HBV) Infection of the Liver Ahmed Mohamed Abdel-B Diab Purdue University
Purdue University Purdue e-Pubs Open Access Dissertations Theses and Dissertations January 2016 The oler of PLK1 in Hepatitis B Virus (HBV) infection of the liver Ahmed Mohamed Abdel-B Diab Purdue University Follow this and additional works at: https://docs.lib.purdue.edu/open_access_dissertations Recommended Citation Diab, Ahmed Mohamed Abdel-B, "The or le of PLK1 in Hepatitis B Virus (HBV) infection of the liver" (2016). Open Access Dissertations. 1214. https://docs.lib.purdue.edu/open_access_dissertations/1214 This document has been made available through Purdue e-Pubs, a service of the Purdue University Libraries. Please contact [email protected] for additional information. Graduate School Form 30 Updated 12/26/2015 PURDUE UNIVERSITY GRADUATE SCHOOL Thesis/Dissertation Acceptance This is to certify that the thesis/dissertation prepared By Ahmed Mohamed Abdel-B Diab Entitled The role of PLK1 in Hepatitis B Virus (HBV) Infection of the Liver For the degree of Doctor of Philosophy Is approved by the final examining committee: Ourania Andrisani Andy W. Tao Co-chair Fabien Zoulim Co-chair Robert Geahlen Xiaoqi Liu To the best of my knowledge and as understood by the student in the Thesis/Dissertation Agreement, Publication Delay, and Certification Disclaimer (Graduate School Form 32), this thesis/dissertation adheres to the provisions of Purdue University’s “Policy of Integrity in Research” and the use of copyright material. Approved by Major Professor(s): Ourania Andrisani Laurie Jaeger 10/6/2016 Approved by: Head of the Departmental Graduate Program Date i THE ROLE OF PLK1 IN HEPATITIS B VIRUS (HBV) INFECTION OF THE LIVER A Dissertation Submitted to the Faculty of Purdue University by Ahmed M Diab In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy December 2016 Purdue University West Lafayette, Indiana ii ACKNOWLEDGEMENTS I would like to begin by extending my gratitude to my committee members Robert Geahlen, Andy W.
[Show full text]