|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for CLDN1(NM_021101.4) Search again
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:
Summary
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial 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 junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. The protein encoded by this gene, a member of the claudin family, is an integral membrane protein and a component of tight junction strands. Loss of function mutations result in neonatal ichthyosis-sclerosing cholangitis syndrome.
Gene References into function
- Claudin-based tight junctions occur in the epidermis and they are crucial for the barrier function of the mammalian skin.
- Involvement in the beta-catenin/Tcf signaling pathway and its frequent upregulation in human colorectal cancers
- CLDN1, clustered with CLDN16 at human chromosome 3q28, is a four-transmembrane protein with WWCC motif, defined by W-X(17-22)-W-X(2)-C-X(8-10)-C.
- Airway tight junctions are regulated by claudin interactions that confer the selectivity of the junction.
- Showed that residues located C-terminal to the last transmembrane domain of claudin 1 are required for the proper targeting to apical TJ.s.
- Lack of claudin-1 in neonatal sclerosing cholangitis syndrome may lead to increased paracellular permeability between epithelial cells and bile duct disease.
- Arrangement of expression and distribution of claudin-1 is closely related to cell dissociation status in pancreatic cancer cells through MEK2 activation
- significant loss of CLDN1 protein in breast cancer cells suggests that CLDN1 may play a role in invasion and metastasis
- This review summarizes the role of claudins in cancer and points out that claudin 1 (CLDN1) may support tumor suppressive functions in tissues such as the brain, where dramatic loss of CLDN1 expression has been demonstrated in glioblastoma multiforme.
- Genetic manipulations of claudin-1 expression in colon cancer cell lines induced changes in cellular phenotype, with structural and functional changes in markers of epithelial-mesenchymal transition.
- Claudin-1 was downregulated by Snail and Slug in MDCK and human breast neoplasm cells.
- 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.
- Differential expression of genes encoding claudins in colorectal cancer suggests that these tight junction proteins may be associated to and involved in tumorigenesis.
- Expression of cytoplasmic claudin-1 was decreased in acute acalculous cholecystitis.
- CLDN1 is required for HCV infection of human hepatoma cell lines and is the first factor to confer susceptibility to HCV when ectopically expressed in non-hepatic cells
- Tight junction proteins contribute to the permeability barrier in epidermal keratinocytes
- Squamous cell carcinomas and carcinoids showed different CLDN1 expression.
- Claudin-1 immunohistochemistry should be considered for use as a new diagnostic tool for distinguishing malignant from benign lesions of the prostate.
- Squamous cell carcinomas were positive for CLDN-1 and negative for CLDN-5, whereas adenocarcinomas were positive for CLDN-5 and negative for CLDN-1.
- CLDN1 expression correlated with the recurrence status and malignant potential of breast cancer.
- Nine potential tetraspanin CD9 partners, including claudin-1, were identified.
- Cell-cell transmission of hepatitis C virus is dependent on CLDN1 expression.
- The expression of claudin-1 and claudin-2 in cancer tissues was upregulated 40- and 49.2-fold, respectively, at the mRNA level, as compared with that in normal tissues
- CLDN1 is unlikely to play a critical role in migration of Langerhans cells (or their precursors) to the epidermis or their positioning within the epidermis.
- Inhibition of claudin-1 expression may represent a novel mechanism that contributes to RON-mediated invasive activities, leading to increased tumor malignancy
- specific localization pattern of CLDN1 may be crucial in the regulation of hepatitis C virus cellular tropism
- in 5 cases of follicular dendritic cell sarcoma, study found diffuse intense positivity of the tumor cells for Glut-1 in all 5 cases and focal and weak immunoreaction for Claudin-1 in 3 cases
- Here, we confirm the role of claudin-1 in HCV entry.
- fluorescent protein-tagged forms of CD81 and CLDN1 colocalized.
- Claudin-1 expression is correlated with recurrence status and poor prognosis in esophageal cancer.
- claudins 1 and 3 had a significant effect on overall survival in patients with urothelial carcinoma of the upper urinary tract.
- Claudin-1 and claudin-2 expression was elevated in active inflammatory bowel disease (IBD), adenomas, and IBD-associated dysplasia, but not acute self limiting colitis
- Suggest that claudin-1 participates in the transformation of biological behaviors in gastric adenocarcinomas.
- For the first time this study proves the presence of Claudin-1, Claudin-3 and Claudin-5 in ECV304 (obtained from ECACC) cell layers and the inducibility of their expression by glioma-conditioned media.
- claudin-1 expression is responsible for TNF-alpha-dependent growth signals and the proliferation of pancreatic cancer cells.
- Mutational study of CLDN1 revealed that its tight junctional distribution plays an important role in mediating hepatitis C virus entry.
- We investigated common genetic variation in CLDN1 in four self-described ethnically distinct U.S. populations to look for genetic variation and signatures of selection and compared CLDN1 with CLDN7, the most similar of the claudin genes.
