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Human Polyclonal CLDN4 Primary Antibody for IF, IHC - ABIN6711708
González-Mariscal, Garay, Quirós: Identification of claudins by western blot and immunofluorescence in different cell lines and tissues. in Methods in molecular biology (Clifton, N.J.) 2011
Show all 2 Pubmed References
Human Polyclonal CLDN4 Primary Antibody for IF (p), IHC (p) - ABIN680743
Wang, Chen, Liang, Yan, Lin, Liu, Luo, Huang, Li, Liu, Tang: Notch inhibition promotes fetal liver stem/progenitor cells differentiation into hepatocytes via the inhibition of HNF-1?. in Cell and tissue research 2014
Human Monoclonal CLDN4 Primary Antibody for FACS - ABIN4895293
Shim, Kim, Jin, Kim, Oh: Claudin 4-targeted nanographene phototherapy using a Clostridium perfringens enterotoxin peptide-photosensitizer conjugate. in Acta pharmacologica Sinica 2018
Human Monoclonal CLDN4 Primary Antibody for CyTOF, FACS - ABIN4898990
Risom, Langer, Chapman, Rantala, Fields, Boniface, Alvarez, Kendsersky, Pelz, Johnson-Camacho, Dobrolecki, Chin, Aswani, Wang, Califano, Lewis, Tomlin, Spellman, Adey, Gray, Sears: Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer. in Nature communications 2019
Antineoplastic cytotoxicity of Clostridium perfringens enterotoxin depends on the conditions of claudin-4 in ovarian carcinoma mouse xenografts.
In our samples, high claudin-4 expression in breast carcinoma-in-situ was more frequent than low expression
Reduced duodenal expression of claudin-4 could be involved in increasing intestinal permeability in acute pancreatitis.
CLDN4 plays a key role in laryngeal squamous carcinoma progression.
Epithelial barrier dysfunction in lymphocytic colitis occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism.
Claudin-4 expression can be absent or very focal in a subset of high-grade endometrial carcinomas
these results suggest that Helicobacter pylori lipopolysaccharide induces TLR2 expression in the gastric adenocarcinoma cells, and that the longer the exposure to lipopolysaccharide, the greater the expression of TLR2 in the cell membrane; consequently the expression of claudin-4, -6, -7 and -9 also increases
HIF-1alpha expression was upregulated in the vasculogenic mimicry-positive CRC cell line HCT-116 and thereby affected the expression of the EMT-related markers Claudin-4, E-cadherin (E-cd) and Vimentin(VIM).
expression of claudin-4 is highly specific for true epithelial differentiation and may be useful to distinguish SWI/SNF complex-deficient undifferentiated carcinomas from sarcomas with epithelioid morphology. The lack of claudin-4 expression in ovarian small cell carcinomas of hypercalcemic type suggests that these tumors may be better regarded as sarcomas rather than carcinomas.
Data indiate a regulatory network in gastric cancer whereby claudin-4 expression is reduced by specific miRNAs, which are in turn bound by specific lncRNAs acting as competing endogenous RNAs (ceRNAs), resulting in increased claudin-4 expression.
This is the first study to show how TGF-beta regulates the expression of Claudin-4 through c-Jun signaling and how this pathway contributes to the migratory and tumorigenic phenotype of lung tumor cells.
Claudin-4 functionally contributes to both ovarian tumor cell apoptosis resistance and migration and targeting extracellular loop interactions of claudin-4 may have therapeutic implications for reducing ovarian tumor burden.
Fluorescence-based flow cytometry and xenon magnetic resonance imaging (MRI) indicate binding of the biosensor specifically to claudin 4 (Cldn4)-expressing cells.
Studies indicate that Grainyhead-like transcription factor 2 (GRHL2) controls the expression of E-cadherin (CDH1) required for adherens junctions and possibly regulates the expression of claudin-4 (CLDN4) in tight junctions.
Studies indicate claudin 1 (CLDN-1) as a target for improving epidermal drug absorption and preventing HCV infection and of claudin 4 (CLDN-4) as a target for anticancer therapeutics.
Mislocalization claudin-3 to nucleus in colon cancer and mislocalization claudin-4 to nucleus in adenomas of the colon were detected for the first time. The potential reasons for the paradoxical expression are discussed and a review of the literature, related all the alleged mechanisms of this mislocalization is provided.
Reg I may play a role in the maintenance of mucosal barrier function by inducing tight junction proteins such as claudins 3 and 4.
claudin-4 may represent different mechanisms of lymphatic vessel invasion with both biomarkers is related to poor prognosis
These results suggested that increase of Cldn4-expression may be involved in early molecular events during carcinogenesis of adenocarcinoma, whereas increase of Cldn7-expression may be associated with tumor invasion or progression.
that claudins-4 and -7 might be valuable markers for distinguishing hepatocellular carcinoma and cholangiocarcinoma and that cholangiolocellular carcinoma might arise from hepatic ductal cells
a Grhl2/Ovol2 network controls Cldn4 and Rab25 expression that facilitates lumen expansion and barrier formation in subtypes of renal epithelia
Data show that claudin-4 and claudin-7 were observed in hepatocytes of severely damaged mouse and human livers.
The claudin-4-mediated chloride conductance can be regulated endogenously by a protease-channel-activating protease 1 (cap1).
Cld4 is selectively expressed on the surface of enteroendocrine cells in the mouse small intestine.
Claudin 4 has little effect on normal lung physiology but may function to protect against acute lung injury in mice.
The results suggest that progressive hydronephrosis in Cldn4(-/-) mice arises from urinary tract obstruction due to urothelial hyperplasia, and that Cld4 plays an important role in maintaining the homeostatic integrity of normal urothelium.
the results indicate that Grhl2 regulates epithelial morphogenesis through transcriptional up-regulation of Cldn3 and Cldn4, as well as of Rab25, which increases the Cldn4 protein and its localization at TJs
Mechanism of Clostridium perfringens enterotoxin interaction with claudin-3/-4 protein suggests structural modifications of the toxin to target specific claudins
Claudin-3 in the apical-most regions maintains the impermeable tight junctions during lactation, and claudin-4 contributes
Claudin-4 overexpression is associated with epigenetic derepression in gastric carcinoma.
results suggest that Cld4 is induced by E-protein activity in the later stages of DP cells to increase the efficiency of positive selection, uncovering a hitherto unrecognized function of a Cld family protein
data show that claudin-4 interacts with claudin-8 and that their association is required for the anion-selective paracellular pathway in the collecting duct
quaternary structure analysis of recombinant protein
Experimental obstructive jaundice increases claudin-4 expression in intestinal epithelium, which may be a key factor contributing to the disruption of the mucosal barrier.
In the absence of follicle-stimulating hormone receptor signaling, claudin-4 is selectively upregulated in ovarian surface epithelium and tumors in comparison to wild type.
Claudin 4 has been found in mouse taste epithelium, with high abundance around the taste pore. A highly specific permeability pattern for paracellular diffusion is apparent, which indicates a peripheral mechanism for taste coding.
Claudin-3 and claudin-4 receptors are highly overexpressed in carcinosarcoma
mouse trophectoderm expressed claudin 4 essential for blastocyst formation in preimplantation mouse embryos
Structural constraints for the binding of short peptides to claudin-4 revealed by surface plasmon resonance.
Tumor necrosis factor-alpha increases claudin-1, 4, and 7 expression in renal tubular cells, altering permeability and transepithelial electrical resistance.
Claudin-4 expression shows age-dependent change in cellular localization on pig jejunal villous epithelial cells
These findings indicate that claudin-4 and -7 may play a role in the gingiva junctional epithelium even in the absence of tight junctions.
This gene encodes an integral membrane protein, which belongs to the claudin family. The protein is a component of tight junction strands and may play a role in internal organ development and function during pre- and postnatal life. This gene is deleted in Williams-Beuren syndrome, a neurodevelopmental disorder affecting multiple systems.
, Clostridium perfringens enterotoxin receptor 1
, Williams-Beuren syndrome chromosomal region 8 protein
, clostridium perfringens enterotoxin receptor
, tight junction-associated protein
, claudin 4