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To gain new insights about the genetic networks controlling hair cell (HC) development, we previously developed a direct genetic programming strategy to generate an inexhaustible supply of HC-like cells (induced HCs, iHCs) in vitro, starting from mouse embryonic stem cells (ESC).
Thus, Math1 seems to be a key transcription factor for HC development.
The molecular mechanisms underlying HC development and differentiation are poorly understood.
Recently, molecular mechanisms related to HC development have been elucidated in detail, while the transcription factor Math1 (also known as Atoh1) has been identified as the earliest HC-specific gene required for definitive HC development.
To investigate the process of generation of HC-like cells from ES cells, we examined the time-course of gene expression related to neural differentiation and HC development in 18-day cultures, which encompassed 4 days for EB formation and the subsequent 14 days for EB outgrowths in ST2-CM.
In an examination of the time-course of gene expression in 18-day cultures of 4-day EBs in regard to neural differentiation and HC development, nestin and myosin7a expressions were the first to appear by day 7, followed by myosin 6 and Math1 by day 11, and Brn3c and α9AchR by day 18, which seemed to mirror the developmental processes of HCs in the cochlea.
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Objective To examine the influence of postnatal energy quotient (EQ, energy intake/kg body weight per day) on head circumference (HC) growth and mental development of very low birth weight (VLBW), small for gestational age (SGA, <10th percentile) preterm infants.
HC developed dignity therapy.
Math1, a basic helix-loop-helix transcription factor homolog of the Drosophila atonal gene, is considered to be a key factor for induction of sensory hair cells (HCs) during development of the organ of Corti or cochlea.
The HC-QI development sample used here is large and international in scope, including home-care clients and agencies in a number of European countries, Canadian provinces, and American states.
The dependence of neurotrophins for the survival and viability of SGNs during these stages has been documented extensively (Fritzsch et al., 2004; Green et al., 2012), but relatively little is known about the mechanisms controlling SGN diversification and wiring with specific cochlear HC regions during development.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com