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Validated All-in-One™ qPCR Primer for CLDN4(NM_001305.4) Search again
Product ID:
HQP002848
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CPE-R, CPER, CPETR, CPETR1, WBSCR8, hCPE-R
Gene Description:
claudin 4
Target Gene Accession:
NM_001305.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- Results support a model in which claudins 2 and 4 create paracellular channels and the first extracellular domain is sufficient to determine both paracellular charge selectivity and transepithelial electrical resistance.
- CLDN4, clustered with CLDN3 at human chromosome 7q11, is a four-transmembrane protein with WWCC motif, defined by W-X(17-22)-W-X(2)-C-X(8-10)-C.
- Claudin-4 is a potent inhibitor of the invasiveness and metastatic phenotype of pancreatic cancer cells, and a target of the transforming growth factor beta and Ras/Raf/extracellular signal-regulated kinase pathways.
- The tail of claudin-2 could stabilize claudin-4, with a concomitant increase in both protein level and physiologic influence.
- claudin 4 may play a role in the disruption of cell-to-cell adhesion in diffuse type gastric cancer and in a loss of differentiation.
- loss of CLDN4 expression in areas of apocrine metaplasia and in the majority of grade 1 invasive carcinomas suggests a particular role for this protein in mammary glandular cell differentiation and carcinogenesis
- tyrosine phosphorylation of claudin-4 attenuates association of claudin-4 with ZO-1, decreasing integration of claudin-4 into sites of cell-cell contact and enhancing paracellular permeability
- The expression of claudin-1, -3 and -4 was upregulated 5.7-, 1.5- and 2.4-fold, respectively, in colorectal tumor tissues in comparison to the normal ones.
- claudin 3 and claudin 4 may play a role in transformation of ovarian surface epithelium towards the malignant phenotype
- Claudin-4 expression seems to be a useful marker in differentiating biliary tract cancers from hepatocellular carcinomas and could well become a potential diagnostic tool.
- Sp1 epigenetic modifications have a critical role in regulation of the CLDN4 promoter in ovarian cancer cells
- WNK1 increases paracellular chloride permeability and phosphorylation of claudin-4
- expression of claudin-4 is lower in diffuse-type gastric cancer than in intestinal-type gastric cancer
- Overexpression of claudin-4 is associated with uterine serous papillary carcinoma
- Tight junction proteins contribute to the permeability barrier in epidermal keratinocytes
- When compared, small-cell-lung cancers and carcinoid tumors, adenocarcinomas, and squamous cell carcinomas in CLDN4 expression.
- Loss of claudin expression may enhance the grade of malignancy of gastric cancer in vivo.
- Claudin-3 and claudin-4 receptors are highly overexpressed in carcinosarcoma
- Our data suggest that JUND and CLDN4 are critical mediators of the antiproliferative and antiviral effects of type I IFNs and further confirm the functional importance of the DNA-binding domain of Stat2.
- The modulation of claudin-4 activity by PKCepsilon may not only provide a mechanism for disrupting TJ function in ovarian cancer, but may also be important in the regulation of TJ function in normal epithelial cells.
- vinculin plays a role in growth regulation of neuroendocrine tumors and in expression of CLD4
- Reduced claudin-4 expression correlates with loss of differentiation in thyroid neoplasms.
- Cdx2 plays an important role in the regulation of intestinal claudin expression not only in gastric mucosa with intestinal metaplasia but also gastric carcinoma.
- MMP-2, MMP-9 and claudin-4 expression may be phenotypic features, distinguishing intestinal-type and diffuse-type gastric cancer.
- Increased expression of claudin-3 and claudin-4 may contribute to aggressive phenotype of endometrial cancer of serous papillary or clear-cell histology. Possible targets for therapeutic intervention.
- Early gastric carcinomas demonstrating I-CLDN(+) phenotype have a high risk of synchronous and metachronous secondary gastric epithelial neoplasias.
- Claudins 1 and 4 expression was significantly associated with stage in patients with urothelial carcinoma of the upper urinary tract.
- Claudin-4, coding for an integral membrane cell-junction protein, was the most significantly (P<0.00001) upregulated marker in both primary and metastatic tumour specimens compared with benign prostatic hyperplasia at both RNA and protein levels
- We found that claudin-4 contains a sequence which is phosphorylated by atypical PKC (aPKC). These findings suggest that aPKC regulates tight junction formation through the phosphorylation of claudin-4.
- Claudin 4 is downregulated in lobular carcinoma in situ compated with normal breast epithelium and stroma.
- The expression of claudins-2, -3 and -4 in 16 rectal well-differentiated endocrine neoplasms was studied