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PDCD5
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Programmed cell death protein 5 (TF-1 cell apoptosis-related protein 19) (Protein TFAR19) [TFAR19] ==Publications== {{medline-entry |title=Correlation of [[PDCD5]] and apoptosis in hair cells and spiral ganglion neurons of different age of C57BL/6J mice. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22282256 |abstract=This study examined the expression pattern of programmed cell death 5 ([[PDCD5]]) in cochlear hair cells and spiral ganglion neurons (SGNs) and its association with age-related hearing loss in mice. Sixty C57BL/6J (C57) mice at different ages were divided into four groups (3, 6, 9 or 12 months). [[PDCD5]] expression was detected by using immunohistochemistry, real-time PCR and Western blot. Morphological change of the cochleae was also evaluated by using immunoassay. The results showed that the expression of [[PDCD5]] had a gradual increase with ageing in both protein and RNA levels in C57 mice, as well as gradually increased apoptosis of cochlear hair cells and SGNs. In addition, we also found that caspase-3 activity was enhanced and its expression was enhanced with ageing. It is implied that overexpression of [[PDCD5]] causes the increase in caspase-3 activity and the subsequent increase of apoptosis in cochlear hair cells and SGNs, and thereby plays a role in the pathogenesis of presbycusis. Thus, [[PDCD5]] may be a new target site for the treatment and prevention of age-related hearing loss. |mesh-terms=* Aging * Animals * Apoptosis Regulatory Proteins * Cells, Cultured * Female * Hair Cells, Auditory * Male * Mice * Mice, Inbred C57BL * Neoplasm Proteins * Spiral Ganglion * Statistics as Topic |full-text-url=https://sci-hub.do/10.1007/s11596-012-0020-z }} {{medline-entry |title=[Expression of [[PDCD5]] and caspase 3 in the cochlea of different age of C57BL/6J mice]. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22177044 |abstract=To investigate the age related changes of the expression of programmed cell death 5 ([[PDCD5]]) and caspase 3 in the cochlea of the different age of C57BL/6J mice. The relationship of [[PDCD5]] and caspase 3 and the possible roles in the pathogenesis of presbycusis were also discussed. C57 mice of 3, 6, 9 and 12 months old were selected and divided into 4 groups, with 15 mice in each group. Auditory function of C57BL/6J mice was measured by auditory brainstem response ([[ABR]]) respectively. The changes of [[PDCD5]] and Caspase 3 protein in the cochlea were detected by immunohistochemistry and Western blotting, the changes of [[PDCD5]] mRNA and caspase 3 mRNA were detected using RT-PCR. With the increase of age, the mean value for [[ABR]] thresholds in response to click, 4 kHz and 8 kHz sound stimulus of C57 mice gradually increased, the expression of [[PDCD5]] and caspase 3 were increased also. At 3 months and 6 months of age in the cochlea of C57, all sorts of expression of [[PDCD5]] and caspase 3 and the expression were enhanced with age. There was an evident expression at 9 months age, but the highest expression was detected at 12 months age. The [[PDCD5]] and Caspase 3 expression were statistically different in each group (P < 0.05). The changes of [[PDCD5]] and caspase 3 mRNA expression were in accordance with that of [[PDCD5]] and Caspase 3 protein expression by the real-time PCR. The expression levels of [[PDCD5]] and caspase 3 in the cochlea of C57 mice increase with age, the results suggested that the expression of [[PDCD5]] and caspase 3 might play an important role in the pathogenic mechanism of presbycusis. |mesh-terms=* Aging * Animals * Apoptosis Regulatory Proteins * Auditory Threshold * Caspase 3 * Cochlea * Mice * Mice, Inbred C57BL * Neoplasm Proteins * Presbycusis }}
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