Title : Dysregulated retinoic acid signaling in airway smooth muscle cells in asthma.

Pub. Date : 2021 Dec

PMID : 34784434






6 Functional Relationships(s)
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1 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens
2 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens
3 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens
4 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens
5 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens
6 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin H19 imprinted maternally expressed transcript Homo sapiens