CLDN9

(redirected from claudin-9)

CLDN9

A gene on chromosome 16p13.3 that encodes claudin-9, an integral membrane protein of the claudin family, the members of which form a physical barrier that prevents solutes and water from passing freely into the interstitial space between epithelial or endothelial cell sheets, and play critical roles in maintaining cell polarity and signal transduction.

Molecular pathology
Claudin-9 is a co-factor for entry of hepatitis C virus; CLDN9 is required for sensory cells in auditory canal; deficiency is associated with deafness.
References in periodicals archive ?
Interestingly, NDRG1 was reported to maintain the integrity of airway epithelial barrier as NDRG1 knockdown significantly decreased claudin-9 expression and impaired the barrier function.[17] However, there were controversial issues about NDRG1 functions.
NDRG1 is important to maintain the integrity of airway epithelial barrier through claudin-9 expression.
The researchers behind the present study have revealed that they used a deaf mouse model, generated at The Jackson Laboratory, to identify the deafness-causing defect in the claudin-9 gene.
They showed that the mutated gene fails to produce normal claudin-9 protein, which is needed to maintain the proper distribution of potassium in the inner ear.
We found that claudin-9 is very important in keeping the amount of potassium on the two sides separate.
The researchers have found that when claudin-9 is mutated, potassium floods the wrong part of the sensory cells, killing most and leaving the remaining ones functionally defective.
In follow-up efforts, the researchers are screening people with hearing impairment to see whether some of them have a mutation in claudin-9.
Background: Claudin-5, claudin-9, and claudin-11 are expressed in endothelial cells to constitute tight junctions, and their deficiency may lead to hyperpermeability, which is the initiating process and pathological basis of cardiovascular disease.
It is extracted, concentrated, and freeze-dried from a group of herbal medicines, such as ginseng, radix paeoniae rubra, borneol, and spiny jujube seed, which contains multiple active components that may be responsible for its antianginal effects.[sup][16],[17],[18] However, the protective mechanism of TXL has not been clarified.[sup][19],[20] Furthermore, we have found that the effect of TXL is on microvascular endothelial cells.[sup][21],[22],[23] Although TXL has been reported to have positive effects on the hypoxia-inhibited claudin-1,[sup][24],[25] whether TXL regulates claudin-5, claudin-9, and claudin-11, which are expressed in the endothelial cells, has not been explored.
To investigate whether TXL modulate claudin-9 and attenuate cell injury in hypoxia, the cells were exposed to hypoxia and treated with TXL and then the messenger RNA (mRNA) expression of claudin-5, claudin-9, and claudin-11 was examined by real-time reverse transcription-polymerase chain reaction (RT-PCR), the claudin-9 protein content was evaluated by western blotting, the claudin-9 distribution was evaluated by immunofluorescence, and cell morphological changes were observed in light microscope.
After the cells had been treated with CoCl[sub]2 (dissolved in phosphate buffered saline [PBS] to a final concentration of 100 [micro]mol/L) to mimic hypoxia,[sup][28] the gene expression of claudin-5, claudin-9, and claudin-11was examined at different time points to verify the optimal hypoxia-stimulation time.