C38 antigen is specifically expressed in neuronal cells of the retina. The purpose of this study was to isolate C38 cDNA and determine its molecular functions. Sequence analysis of C38 cDNA revealed that C38 is equivalent to rat BM88, which has been reported to induce cell-cycle arrest and neuronal differentiation in Neuro2a cells. C38 and Ki67, a marker of proliferating cells, were not colocalized during retinal development. C38 was first detected in the retinal ganglion cells at embryonic day 16, much later than the expression of doublecortin, a marker of immature neurons. Although all the horizontal cells were post-mitotic at this stage, C38 was not detected in horizontal cells until the postnatal period. In addition, C38 over-expression did not induce neuronal differentiation or cell-cycle arrest of pluripotent P19 embryonal carcinoma cells. Instead, C38 promoted maturation during neuronal differentiation of P19 embryonal carcinoma cells by down-regulating Oct-3, a pluripotent cell marker and enhancing the expressions of positive regulators of neurogenesis. In conclusion, during retinal development, C38 is first expressed in post-mitotic retinal neurons and is up-regulated during their maturation. C38 does not induce neuronal competence in pluripotent cells, but does promote maturation in already committed neuronal cells.
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http://dx.doi.org/10.1111/j.1471-4159.2009.06536.x | DOI Listing |
Respir Res
January 2025
Instituto Universitario de Enfermedades Tropicales y Salud Pública de Canarias (IUETSPC), Universidad de La Laguna, San Cristóbal de La Laguna, Tenerife, Spain.
Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow obstruction and destruction of lung tissue, primarily attributed to tobacco smoking. However, other factors like biomass-burning smoke (BS) exposure are also implicated. COPD has been described as an accelerated aging disease, and telomere length is a biomarker of aging.
View Article and Find Full Text PDFEcon Educ Rev
August 2024
Department of Economics, Texas A&M University.
We use data from a randomized early childhood education program to estimate the production technology of early life skills. Estimates indicate that, for more disadvantaged children, parental investment is a more effective input for producing skills than childcare. The reverse is true for the more advantaged.
View Article and Find Full Text PDFAquac Nutr
November 2024
Laboratory of Aquaculture Nutrition and Environmental Health, School of Life Sciences, East China Normal University, Shanghai 200241, China.
A 50-day test was adopted to compare the growth performance, liver histology, glucose metabolism, lipid (L) metabolism, ion transport, and ammonia metabolism of tilapia fed different carbohydrate-lipid (C:L) ratio diets under saline-alkaline water (salinity = 16 mmol/L and alkalinity = 35 mmol/L). The C and L levels of five isoenergetic (16.5 kJ/g) and isonitrogenous (32% protein) diets were C45%:L3% (L3), C38%:L6% (L6), C31%:L9% (L9), C24%:L12% (L12), and C17%:L15% (L15).
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
State Key Laboratory of Resource Insects, Southwest University, Chongqing, China. Electronic address:
The plant apoplast is a key battleground in the initial stages of interaction between the plant and pathogen. Despite its importance, few apoplastic effectors have been characterized to date. Here, we identified Ssh1296, a conserved apoplastic effector from Scleromitrula shiraiana.
View Article and Find Full Text PDFNeurol Sci
October 2024
Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Introduction: Sexual dysfunction manifests as various challenges during sexual activity and is a prevalent condition that significantly impacts quality of life. Post stroke sexual dysfunction (PSSD) is particularly concerning, yet it is often overlooked by both healthcare providers and patients.
Methods: We conducted a comprehensive literature review, examining research and reports related to sexual dysfunction following stroke.
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