Recently, Yang et al. reported that estrogen receptor beta (ERbeta) is a mitochondrial protein rather than a nuclear receptor. Because this claim would lead to a significant change in our understanding of estrogen signaling, we have attempted to reproduce the MALDI-TOF data of Yang et al. We separated proteins extracted from mouse liver mitochondria by SDS-PAGE and analysed a gel band covering the molecular weight range of 50-65 kDa by MALDI-TOF/TOF. Analysis of the data with the MASCOT database algorithm provided no evidence for the presence of ERbeta in the mitochondria. If we search (as the authors did) with only the peptide masses which match to tryptic fragments of ERbeta, ERbeta is identified with a significant score of 69. However, fragmentation of these peptides shows that they are not from ERbeta. Our conclusion is that ERbeta cannot be identified by MALDI-TOF from a mixture of mitochondrial proteins resolved on SDS-PAGE.
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http://dx.doi.org/10.1016/j.bbrc.2006.02.164 | DOI Listing |
Exp Gerontol
January 2025
Department of Biological Sciences, University of Limerick, Limerick V94 T9PX, Ireland. Electronic address:
The increasing prevalence of Alzheimer's disease (AD) calls for a comprehensive exploration of its complex etiology, with a focus on sex-specific vulnerability, particularly the heightened susceptibility observed in postmenopausal women. Neurometabolic alterations during the endocrine transition emerge as early indicators of AD pathology, including reduced glucose metabolism and increased amyloid-beta (Aβ) deposition. The fluctuating endocrine environment, marked by declining estradiol levels and reduced estrogen receptor beta (ERβ) activity, further exacerbates this process.
View Article and Find Full Text PDFJ Cell Physiol
January 2025
School of Biological Sciences, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Estrogen is an essential hormone for the development and functional activities of reproductive organs. Recent studies showed that estrogen signaling is also an important regulator of lipid and glucose metabolism in a number of tissues, but the molecular mechanism is not fully understood. We report here that estrogen is a stimulator of brain-derived neurotrophic factor (BDNF) synthesis in the skeletal muscle.
View Article and Find Full Text PDFAutophagy
November 2024
Department of Biochemistry and Molecular Biology, University of New Mexico, Albuquerque, NM, USA.
Mitophagy, the process by which cells eliminate damaged mitochondria, is mediated by PINK1 (PTEN induced kinase 1). Our recent research indicates that PINK1 functions as a tumor suppressor in colorectal cancer by regulating cellular metabolism. Interestingly, PINK1 ablation activated the NLRP3 (NLR family pyrin domain containing 3) inflammasome, releasing IL1B (interleukin 1 beta).
View Article and Find Full Text PDFNeurochem Int
October 2023
Institute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, 271021, China. Electronic address:
Zhejiang Da Xue Xue Bao Yi Xue Ban
March 2024
Department of TCM Gynecology, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou 310007, China.
Objectives: To investigate the effect of Chinese medicine He's Yangchao recipe on premature ovarian insufficiency (POI) and its relationship with mitochondrial function of ovarian granulose cells in an animal model.
Methods: Thirty-six female C57BL/6J mice were randomly divided into blank control group, model group, low-, medium- and high-dose He's Yangchao recipe treatment group and coenzyme Q10 (Q10) treatment group (positive control). The POI model was induced by a single intraperitoneal injection of cyclophosphamide (90 mg/kg).
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