C
Chen-Che Jeff Huang
Researcher at Auburn University
Publications - 19
Citations - 379
Chen-Che Jeff Huang is an academic researcher from Auburn University. The author has contributed to research in topics: Adrenal cortex & Steroidogenic factor 1. The author has an hindex of 9, co-authored 16 publications receiving 309 citations. Previous affiliations of Chen-Che Jeff Huang include University of Illinois at Urbana–Champaign & Academia Sinica.
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Progenitor Cell Expansion and Organ Size of Mouse Adrenal Is Regulated by Sonic Hedgehog
TL;DR: The results provide the genetic evidence to support that the adrenal capsule contributes to the growth of adrenocortex in both fetal and adult life but also identify a novel role of Shh in this process.
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Histone Deacetylase Inhibitors Reduce Steroidogenesis through SCF-Mediated Ubiquitination and Degradation of Steroidogenic Factor 1 (NR5A1)
Wei Yi Chen,Jui Hsia Weng,Jui Hsia Weng,Chen-Che Jeff Huang,Chen-Che Jeff Huang,Bon Chu Chung,Bon Chu Chung +6 more
TL;DR: It is shown that HDAC inhibitors suppressed the expression of steroidogenic gene CYP11A1 and decreased steroid secretion by increasing the ubiquitination and degradation of SF-1, a factor important for the transcription of all steroidogenic genes and is the cause of the reduction in steroidogenesis caused byHDAC inhibitors.
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Inactivation of Dicer1 in Steroidogenic factor 1-positive cells reveals tissue-specific requirement for Dicer1 in adrenal, testis, and ovary.
TL;DR: Dicer1 is dispensable for formation and differentiation of fetal tissues derived from the SF1-positive adrenogonadal primordium and development of the ovary from fetal stages to postnatal day 5 does not require the presence of Dicer1.
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Fetal Glucocorticoid Synthesis Is Required for Development of Fetal Adrenal Medulla and Hypothalamus Feedback Suppression
TL;DR: The data indicate blunted feedback suppression despite reasonable amounts of circulating corticosterone, which is required for negative feedback suppression of the hypothalamus-pituitary-adrenal axis and for catecholamine synthesis in adrenal medulla.
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Mutation of Mouse Cyp11a1 Promoter Caused Tissue-Specific Reduction of Gene Expression and Blunted Stress Response without Affecting Reproduction
Meng Chun Shih,Nai Chi Hsu,Nai Chi Hsu,Chen-Che Jeff Huang,Tzong Shoon Wu,Pao Yen Lai,Pao Yen Lai,Bon Chu Chung +7 more
TL;DR: CYP11A1 appears in normal mice to be expressed above the minimal required level, providing a large capacity for use in response to stress, and results in reduced stress response due to decreased adrenal CYP11a1 expression and insufficient stress-induced glucocorticoids secretion.