CLDN3 Rabbit Pab

Leader in Biomolecular Solutions for Life Science CLDN3 Rabbit pAb Catalog No.: A11650 Basic Information Background Catalog No. Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial A11650 cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These Observed MW junctions are comprised of sets of continuous networking strands in the outwardly 27kDa facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. The protein encoded by this intronless gene, a member of the Calculated MW claudin family, is an integral membrane protein and a component of tight junction 23kDa strands. It is also a low-affinity receptor for Clostridium perfringens enterotoxin, and shares aa sequence similarity with a putative apoptosis-related protein found in rat. Category Primary antibody Applications WB Cross-Reactivity Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 1365 O15551 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 141-220 of human CLDN3 (NP_001297.1). Synonyms CLDN3;C7orf1;CPE-R2;CPETR2;HRVP1;RVP1;claudin-3 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using CLDN3 antibody (A11650) at 1:3000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 20s. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

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Gene Expression Is Related to Parental Origin and Regional Coordinate Control
Journal of Human Genetics (2009) 54, 193–198 & 2009 The Japan Society of Human Genetics All rights reserved 1434-5161/09 $32.00 www.nature.com/jhg ORIGINAL ARTICLE William’s syndrome: gene expression is related to parental origin and regional coordinate control Jeremy C Collette1, Xiao-Ning Chen1, Debra L Mills2, Albert M Galaburda3, Allan L Reiss4, Ursula Bellugi5 and Julie R Korenberg1,6 William’s syndrome (WS) features a spectrum of neurocognitive and behavioral abnormalities due to a rare 1.5 MB deletion that includes about 24–28 genes on chromosome band 7q11.23. Study of the expression of these genes from the single normal copy provides an opportunity to elucidate the genetic and epigenetic controls on these genes as well as their roles in both WS and normal brain development and function. We used quantitative RT-PCR to determine the transcriptional level of 14 WS gene markers in a cohort of 77 persons with WS and 48 normal controls. Results reported here: (1) show that the expression of the genes deleted in WS is decreased in some but not all cases, (2) demonstrate that the parental origin of the deletion contributes to the level of expression of GTF2I independently of age and gender and (3) indicate that the correlation of expression between GTF2I and some other genes in the WS region differs in WS subjects and normal controls, which in turn points toward a regulatory role for this gene. Interspecies comparisons suggest GTF2I may play a key role in normal brain development. Journal of Human Genetics (2009) 54, 193–198; doi:10.1038/jhg.2009.5; published online 13 March 2009 Keywords: William’s syndrome; gene expression; RT-PCR; parental origin; GTF2I INTRODUCTION As an approach toward understanding the role of the deleted genes William’s syndrome (WS) is a neurogenetic disorder affecting human in WS, we have characterized WS subjects according to genetic, social/ development and adult cognition.
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Salinity Regulates Claudin Mrna and Protein Expression in the Teleost Gill
View metadata, citation and similar papers at core.ac.uk brought to you by CORE Am J Physiol Regul Integr Comp Physiol 294: R1004–R1014, 2008. provided by University of Southern Denmark Research Output First published January 9, 2008; doi:10.1152/ajpregu.00112.2007. Salinity regulates claudin mRNA and protein expression in the teleost gill Christian K. Tipsmark,* David A. Baltzegar,* Ozkan Ozden, Brenda J. Grubb, and Russell J. Borski Department of Zoology, North Carolina State University, Raleigh, North Carolina Submitted 14 February 2007; accepted in final form 19 December 2007 Tipsmark CK, Baltzegar DA, Ozden O, Grubb BJ, Borski RJ. The biochemical basis for changes in water permeability may Salinity regulates claudin mRNA and protein expression in the teleost entail the robust downregulation of gill aquaporin mRNA and gill. Am J Physiol Regul Integr Comp Physiol 294: R1004–R1014, 2008. protein expression that accompanies SW acclimation in eel (6, First published January 9, 2008; doi:10.1152/ajpregu.00112.2007.—The 21). Although osmotic permeability decreases in SW, the teleost gill carries out NaCl uptake in freshwater (FW) and NaCl conductance and short-circuit current is found to be larger in a excretion in seawater (SW). This transformation with salinity requires close regulation of ion transporter capacity and epithelial permeabil- SW teleost compared with a FW fish (8, 27). A simultaneous change in the ultrastructure of tight junctions (TJs) is also seen Downloaded from ity. This study investigates the regulation of tight-junctional claudins ϩ during salinity acclimation in fish. We identified claudin 3- and (28). Secretion of Na is thought to involve a paracellular claudin 4-like immunoreactive proteins and examined their expression path confined to thin “leaky” TJs that occur in SW between and that of select ion transporters by performing Western blot in mature chloride cells and accessory cells (19, 36), and this tilapia (Oreochromis mossambicus) gill during FW and SW acclima- may contribute to the relatively high ionic permeability of tion.
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Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
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Claudin-1, -3 and -4 Proteins and Mrna Expression in Benign and Malignant Breast Lesions: a Research Study
Available online http://breast-cancer-research.com/content/7/2/R296 ResearchVol 7 No 2 article Open Access Claudin-1, -3 and -4 proteins and mRNA expression in benign and malignant breast lesions: a research study Anna-Mária Tőkés1*, Janina Kulka1*, Sándor Paku2, Ágnes Szik1, Csilla Páska1, Pál Kaposi Novák1, László Szilák1, András Kiss1, Krisztina Bögi1 and Zsuzsa Schaff1 12nd Department of Pathology, Semmelweis University, Budapest, Hungary 2Department of Molecular Pathology, Joint Research Organization of the Hungarian Academy of Sciences, Budapest, Hungary * Contributed equally Corresponding author: Janina Kulka, [email protected] Received: 23 Jan 2004 Revisions requested: 15 Mar 2004 Revisions received: 1 Oct 2004 Accepted: 2 Dec 2004 Published: 31 Jan 2005 Breast Cancer Research 2005, 7:R296-R305 (DOI 10.1186/bcr983)http://breast-cancer-research.com/content/7/2/R296 © 2005 Tőkés et al., licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/ 2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is cited. Abstract Introduction We compared levels of protein and mRNA CLDN4 was present in all 56 tissue sections. However, CLDN4 expression of three members of the claudin (CLDN) family in was highly positive in normal epithelial cells and was decreased malignant breast tumours and benign lesions. or absent in 17 out of 21 ductal carcinoma grade 1, in special types of breast carcinoma (mucinous, papillary, tubular) and in Methods Altogether, 56 sections from 52 surgically resected areas of apocrine metaplasia.
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Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders
177 Arch Neuropsychitry 2020;57:177−191 RESEARCH ARTICLE https://doi.org/10.29399/npa.24890 Chromosomal Microarray Analysis in Turkish Patients with Unexplained Developmental Delay and Intellectual Developmental Disorders Hakan GÜRKAN1 , Emine İkbal ATLI1 , Engin ATLI1 , Leyla BOZATLI2 , Mengühan ARAZ ALTAY2 , Sinem YALÇINTEPE1 , Yasemin ÖZEN1 , Damla EKER1 , Çisem AKURUT1 , Selma DEMİR1 , Işık GÖRKER2 1Faculty of Medicine, Department of Medical Genetics, Edirne, Trakya University, Edirne, Turkey 2Faculty of Medicine, Department of Child and Adolescent Psychiatry, Trakya University, Edirne, Turkey ABSTRACT Introduction: Aneuploids, copy number variations (CNVs), and single in 39 (39/123=31.7%) patients. Twelve CNV variant of unknown nucleotide variants in specific genes are the main genetic causes of significance (VUS) (9.75%) patients and 7 CNV benign (5.69%) patients developmental delay (DD) and intellectual disability disorder (IDD). were reported. In 6 patients, one or more pathogenic CNVs were These genetic changes can be detected using chromosome analysis, determined. Therefore, the diagnostic efficiency of CMA was found to chromosomal microarray (CMA), and next-generation DNA sequencing be 31.7% (39/123). techniques. Therefore; In this study, we aimed to investigate the Conclusion: Today, genetic analysis is still not part of the routine in the importance of CMA in determining the genomic etiology of unexplained evaluation of IDD patients who present to psychiatry clinics. A genetic DD and IDD in 123 patients. diagnosis from CMA can eliminate genetic question marks and thus Method: For 123 patients, chromosome analysis, DNA fragment analysis alter the clinical management of patients. Approximately one-third and microarray were performed. Conventional G-band karyotype of the positive CMA findings are clinically intervenable.
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Single Cell Transcriptional and Chromatin Accessibility Profiling Redefine Cellular Heterogeneity in the Adult Human Kidney
ARTICLE https://doi.org/10.1038/s41467-021-22368-w OPEN Single cell transcriptional and chromatin accessibility profiling redefine cellular heterogeneity in the adult human kidney Yoshiharu Muto 1,7, Parker C. Wilson 2,7, Nicolas Ledru 1, Haojia Wu1, Henrik Dimke 3,4, ✉ Sushrut S. Waikar 5 & Benjamin D. Humphreys 1,6 1234567890():,; The integration of single cell transcriptome and chromatin accessibility datasets enables a deeper understanding of cell heterogeneity. We performed single nucleus ATAC (snATAC- seq) and RNA (snRNA-seq) sequencing to generate paired, cell-type-specific chromatin accessibility and transcriptional profiles of the adult human kidney. We demonstrate that snATAC-seq is comparable to snRNA-seq in the assignment of cell identity and can further refine our understanding of functional heterogeneity in the nephron. The majority of differ- entially accessible chromatin regions are localized to promoters and a significant proportion are closely associated with differentially expressed genes. Cell-type-specific enrichment of transcription factor binding motifs implicates the activation of NF-κB that promotes VCAM1 expression and drives transition between a subpopulation of proximal tubule epithelial cells. Our multi-omics approach improves the ability to detect unique cell states within the kidney and redefines cellular heterogeneity in the proximal tubule and thick ascending limb. 1 Division of Nephrology, Department of Medicine, Washington University in St. Louis, St. Louis, MO, USA. 2 Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO, USA. 3 Department of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. 4 Department of Nephrology, Odense University Hospital, Odense, Denmark.
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Supplementary Data
Supplemental figures Supplemental figure 1: Tumor sample selection. A total of 98 thymic tumor specimens were stored in Memorial Sloan-Kettering Cancer Center tumor banks during the study period. 64 cases corresponded to previously untreated tumors, which were resected upfront after diagnosis. Adjuvant treatment was delivered in 7 patients (radiotherapy in 4 cases, cyclophosphamide- doxorubicin-vincristine (CAV) chemotherapy in 3 cases). 34 tumors were resected after induction treatment, consisting of chemotherapy in 16 patients (cyclophosphamide-doxorubicin- cisplatin (CAP) in 11 cases, cisplatin-etoposide (PE) in 3 cases, cisplatin-etoposide-ifosfamide (VIP) in 1 case, and cisplatin-docetaxel in 1 case), in radiotherapy (45 Gy) in 1 patient, and in sequential chemoradiation (CAP followed by a 45 Gy-radiotherapy) in 1 patient. Among these 34 patients, 6 received adjuvant radiotherapy. 1 Supplemental Figure 2: Amino acid alignments of KIT H697 in the human protein and related orthologs, using (A) the Homologene database (exons 14 and 15), and (B) the UCSC Genome Browser database (exon 14). Residue H697 is highlighted with red boxes. Both alignments indicate that residue H697 is highly conserved. 2 Supplemental Figure 3: Direct comparison of the genomic profiles of thymic squamous cell carcinomas (n=7) and lung primary squamous cell carcinomas (n=6). (A) Unsupervised clustering analysis. Gains are indicated in red, and losses in green, by genomic position along the 22 chromosomes. (B) Genomic profiles and recurrent copy number alterations in thymic carcinomas and lung squamous cell carcinomas. Gains are indicated in red, and losses in blue. 3 Supplemental Methods Mutational profiling The exonic regions of interest (NCBI Human Genome Build 36.1) were broken into amplicons of 500 bp or less, and specific primers were designed using Primer 3 (on the World Wide Web for general users and for biologist programmers (see Supplemental Table 2) [1].
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CLDN3 Expression and Function in Pregnancy‑Induced Hypertension
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Loss of CLDN5 in Podocytes Deregulates WIF1 to Activate WNT Signaling and Contributes to Kidney Disease
Loss of CLDN5 in podocytes deregulates WIF1 to activate WNT signaling and contributes to kidney disease Jie Yan Binzhou Medical Univeristy Hui Li Qingdao University Hui Sun Hebei Medical University Haotian Guo Chinese Academy of Sciences Jieying Liu Binzhou Medical University Mingxia Wang Binzhou Medical University Ninghua Lin Binzhou Medical University Xiangdong Wang Binzhou Medical University Xin Wang Qingdao University Li Li Binzhou Medical University Yongfeng Gong ( [email protected] ) Binzhou Medical Univeristy Article Keywords: kidney disease, WNT activity, CLDN5, WIF1 Posted Date: March 13th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-285550/v1 Page 1/27 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 2/27 Abstract Although mature podocytes lack tight junctions (TJs) and form slit diaphragms between opposing foot processes, TJ integral membrane protein CLDN5 is predominantly expressed throughout the plasma membrane of podocytes under normal conditions. Here using podocyte specic Cldn5 knockout mice as a model, we identify CLDN5 as a crucial regulator of podocyte function and reveal Cldn5 deletion exacerbates podocyte injury and proteinuria in diabetic nephropathy (DN) mouse model. Mechanistically, CLDN5 absence reduces ZO1 expression and induces the nuclear translocation of ZONAB, followed by transcriptional downregulation of WIF1, which leads to activation of WNT signaling pathway. Knockout Wif1 in podocytes result in the development of proteinuria and typical glomerular ultrastructure change occurring in Cldn5 knockout mice, while targeted delivery of Wif1 to podocytes prevents the development of glomerular nephropathy in Cldn5 knockout diabetic mice. Podocyte-derived WIF1 also plays a paracrine role on tubular epithelial cells, evidenced by animals with podocyte deletion of Cldn5 or Wif1 have worse kidney brosis after unilateral ureteral obstruction when compared with littermate controls with intact podocyte WIF1 expression.
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Morphologic Determinant of Tight Junctions Revealed by Claudin-3 Structures
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Claudins 1, 3, 4, 7 and 10-Year Survival in Triple-Negative Breast Tumors
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