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kinetin/atrophy

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The inhibition of kohlrabi chloroplast degeneration by kinetin.

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Kinetin inhibits apoptosis of aging spleen cells induced by D-galactose in rats.

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Kinetin (Kn) is a cytokinin growth factor that exerts several anti-aging and antioxidant effects on cells and organs. To investigate the mechanism underlying apoptotic events in aging cells induced by D-galactose (D-gal), we examined the effect of Kn delivered via nuchal subcutaneous injection on
Small pieces of tissue from the basal, equatorial, near-apical, and apical regions of the third turgid onion leaf base were treated (3 and 6 h in the dark) with abscisic acid (ABA), gibberellic acid (GA3), indoleacetic acid (IAA), and kinetin (K) and compared with responses in water controls. ABA

Long-term oral kinetin does not protect against α-synuclein-induced neurodegeneration in rodent models of Parkinson's disease.

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Mutations in the mitochondrial kinase PTEN-induced putative kinase 1 (PINK1) cause Parkinson's disease (PD), likely by disrupting PINK1's kinase activity. Although the mechanism(s) underlying how this loss of activity causes degeneration remains unclear, increasing PINK1 activity may therapeutically

Effects of kinetin on plant growth and chloroplast ultrastructure of two Pteris species under arsenate stress.

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Cytokinins (CTKs) are effective in alleviating abiotic stresses on plants, but little information is available regarding the effects of CTKs on arsenic (As) accumulation and changes of chloroplast ultrastructure in plants with different As-accumulating ability. Here a hydroponic experiment was

Substituted nitroguanidines provide cytokinin activity during in vitro cultivation of plant tissues.

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Synthetic nitroguanidine derivatives can be used as alternatives to the traditional adenine-containing cytokinins used in plant tissue culture. First, nitroguanidine derivatives (NG) mimicked the typical activity of two standard cytokinins, 6-benzylaminopurine (BAP) and 2-isopentenyladenine (2iP) in

Olfactory stem cells, a new cellular model for studying molecular mechanisms underlying familial dysautonomia.

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BACKGROUND Familial dysautonomia (FD) is a hereditary neuropathy caused by mutations in the IKBKAP gene, the most common of which results in variable tissue-specific mRNA splicing with skipping of exon 20. Defective splicing is especially severe in nervous tissue, leading to incomplete development
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