HuR drives lung fibroblast differentiation but not metabolic reprogramming in response to TGF-β and hypoxia
Joshua Trivlidis; Noof Aloufi; Fatmah Al-Habeeb; Parameswaran Nair; Ilan Azuelos; David H. Eidelman; Carolyn J. Baglole · 2021 · Respiratory Research
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Abstract Background Pulmonary fibrosis is thought to be driven by recurrent alveolar epithelial injury which leads to the differentiation of fibroblasts into α-smooth muscle actin (α-SMA)-expressing myofibroblasts and subsequent deposition of extracellular matrix (ECM). Transforming growth factor beta-1 (TGF-β1) plays a key role in fibroblast differentiation, which we have recently shown involves human antigen R (HuR). HuR is an RNA binding protein that also increases the translation of hypoxia inducible factor (HIF-1α) mRNA, a transcription factor critical for inducing a metabolic shift from
Abstract by Joshua Trivlidis; Noof Aloufi; Fatmah Al-Habeeb; Parameswaran Nair; Ilan Azuelos; David H. Eidelman; Carolyn J. Baglole, Respiratory Research (2021) — licensed CC BY 4.0.
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Metadata source: DOAJ · DOI 10.1186/s12931-021-01916-4
