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Publisher Correction: Intestinal Nogo-B reduces GLP1 levels by binding to proglucagon on the endoplasmic reticulum to inhibit PCSK1 cleavage.
Nat Commun
September 2024
Department of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Correction to: Nogo-B receptor increases glycolysis and the paclitaxel resistance of estrogen receptor-positive breast cancer via the HIF-1α-dependent pathway.
Cancer Gene Ther
May 2023
Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
[Corrigendum] Nogo‑B promotes the epithelial‑mesenchymal transition in HeLa cervical cancer cells via Fibulin‑5.
Oncol Rep
May 2022
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Hubei, Wuhan 430072, P.R. China.
Following the publication of the above article, an interested reader drew to the authors' attention that the 'NB‑4' and 'NB‑2' panels for the invasion and migration assays shown in Fig. 3B and C on p. 113 appeared to contain overlapping data, such that the data may have been derived from the same original source, even though the panels were intending to have shown results obtained under different experimental conditions.
View Article and Find Full Text PDFRosiglitazone alleviates intrahepatic cholestasis induced by α-naphthylisothiocyanate in mice: The role of circulating 15-deoxy-Δ -PGJ and Nogo.
Br J Pharmacol
March 2020
Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, College of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Background And Purpose: Intrahepatic cholestasis is mainly caused by dysfunction of bile secretion and has limited effective treatment. Rosiglitazone is a synthetic agonist of PPARγ, whose endogenous agonist is 15-deoxy-Δ -PGJ (15d-PGJ ). Reticulon 4B (Nogo-B) is the detectable Nogo protein family member in the liver and secreted into circulation.
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