Molecular and Cellular Endocrinology
(MOL CELL ENDOCRINOL ) 《分子与细胞内分泌学 》
2015年影响因子
3.859
期刊介绍
"Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
The journal is fulfilling this aim by publishing full-length original research papers, rapid papers, invited reviews, At the Cutting Edge essays, and book reviews."
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目录导读
Published 2012年11月,Volume 364,Issue 1-2
最新一期
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The molecular mechanisms of pancreatic β-cell glucotoxicity: Recent findings and future research directionsReview ArticlePages 1-27 Mohammed Bensellam, D. Ross Laybutt, Jean-Christophe Jonas  Show preview | Related articles | Related reference work articles
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Regular Papers
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C/EBPα promotes transcription of the porcine perilipin5 geneOriginal Research ArticlePages 28-35 Lei Zhou, Lijie Zhang, Qingjie Meng, Congcong Niu, Dan Jin, An Yu, Li Gan, Zaiqing Yang Show preview | Related articles | Related reference work articles
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Highlights
► C/EBPα is a crucial regulatory factor for plin5 transcription. ► C/EBPα binds to the promoter of plin5 within the −302 to −284 bp region. ► C/EBPα promotes expression of endogenous plin5. ► C/EBPα may be involved in transcriptional regulation of plin5 during fasting.
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Reduced insulin secretion correlates with decreased expression of exocytotic genes in pancreatic islets from patients with type 2 diabetesOriginal Research ArticlePages 36-45 Sofia A. Andersson, Anders H. Olsson, Jonathan L.S. Esguerra, Emilia Heimann, Claes Ladenvall, Anna Edlund, Albert Salehi, Jalal Taneera, Eva Degerman, Leif Groop, Charlotte Ling, Lena Eliasson Show preview |  PDF (824 K) |
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Highlights
► Expression of STX1A, SYT4, SYT7, SYT11 and SYT13 is reduced in islets from human T2D donors. ► Expression of STX1A, SYT4,SYT7, SYT11, SYT13, SNAP25 and STXBP1 correlates positively with GSIS. ► Expression of STX1A, SYT4, SYT7, SYT11, SYT13,SNAP25 and STXBP1 correlates negatively to HbA1c. ► Reduced expression of exocytotic genes contribute to impaired insulin secretion.
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GLP-2 receptors in human disease: High expression in gastrointestinal stromal tumors and Crohn’s diseaseOriginal Research ArticlePages 46-53 Meike Körner, Ruth Rehmann, Jean Claude Reubi Show preview | Related articles | Related reference work articles
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Highlights
► GLP-2 has been linked to carcinogenesis. ► The GLP-2 analogue teduglutide reduces inflammation in Crohn’s disease patients. ► We found GLP-2 receptors in GIST tumor cells and in myenteric nerves in Crohn. ► GLP-2 receptors in GIST may be in vivo targets for radioactive GLP-2 analogs. ► The myenteric GLP-2 receptors may be teduglutide targets in Crohn’s disease.
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Regulation of CYP3A4 and CYP3A5 expression and modulation of “intracrine” metabolism of androgens in prostate cells by liganded vitamin D receptorOriginal Research ArticlePages 54-64 Orla Maguire, Catherine Pollock, Philip Martin, Andrew Owen, Thomas Smyth, Declan Doherty, Moray J. Campbell, Stephen McClean, Paul Thompson Show preview |
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Highlights
► The vitamin D hormone enhances CYP3A4 and CYP3A5 expression within prostate cells. ► Vitamin D regulation of CYP3A4 andCYP3A5 was directly mediated through VDR. ► Vitamin D treatment increased CYP3A enzyme activity with LNCaP cells. ► Elevated CYP3A function increased the intracellular inactivation of testosterone.
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β-Arrestin1-mediated recruitment of c-Src underlies the proliferative action of glucagon-like peptide-1 in pancreatic β INS832/13 cellsOriginal Research ArticlePages 65-70 Jason Talbot, Erik Joly, Marc Prentki, Jean Buteau Show preview | Related articles | Related reference work articles
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Highlights
► GLP-1 enhances c-Src activity. ► GLP-1 triggers the formation of a signaling complex comprising β-arrestin1 and c-Src. ► β-Arrestin1 and c-Src mediates the action of GLP-1 on β-cell proliferation.
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Normal testicular function without detectable follicle-stimulating hormone. A novel mutation in the follicle-stimulating hormone receptor gene leading to apparent constitutive activity and impaired agonist-induced desensitization and internalizationOriginal Research ArticlePages 71-82 Patricia Casas-González, Hugo E. Scaglia, Marco A. Pérez-Solís, Guillaume Durand, Javier Scaglia, Teresa Zariñán, James A. Dias, Eric Reiter, Alfredo Ulloa-Aguirre Show preview |
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Highlights
► We report a novel mutation in the follicle-stimulating hormone receptor. ► The N431I mutation in the FSHR leads to constitutive activation. ► The N431I mutation in the FSHR leads to impaired desensitization. ► The N431I mutation in the FSHR leads to impaired internalization. ► The mutation (N431I) was detected in an asyntomatic man with normal spermatogenesis.
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Estrogen and telomerase in human peripheral blood mononuclear cellsOriginal Research ArticlePages 83-88 Ann L. Benko, Nancy J. Olsen, William J. Kovacs Show preview | Related articles | Related reference work articles
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Highlights
► We evaluated a postulated role for estrogens in regulation of telomerase in T lymphocytes. ► T cells from females showed slightly greater telomerase induction with T cell receptor engagement. ► Estradiol did not directly change telomerase activity in resting or activated T cells. ► Our experiments exclude a direct effect of estradiol on telomerase induction in peripheral T cells.
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Experimental and computational study of inter- and intra- species specificity of gonadotropins for various gonadotropin receptorsOriginal Research ArticlePages 89-100 Joseph Aizen, Noga Kowalsman, Makito Kobayashi, Lian Hollander, Young Chang Sohn, Goro Yoshizaki, Masha Y. Niv, Berta Levavi-Sivan Show preview |
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Highlights
► The article presents molecular modeling of GTHs and GTHRs of tilapia, trout and eel. ► Each of the gonadotropins of eel, trout tilapia and human activated its own cognate receptors. ► Tilapia LHR was activated by hCG and eel LHR was activated by hFSH, hCG, and trout FSH. ► For FSHR, the only cross-reactivity detected was for hFSHR, which was activated by pFSH and bFSH.
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Efficacy of the novel dual PI3-kinase/mTOR inhibitor NVP-BEZ235 in a preclinical model of adrenocortical carcinomaOriginal Research ArticlePages 101-104 Mabrouka Doghman, Enzo Lalli Show preview | Related articles | Related reference work articles
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Highlights
► Current therapies for advanced adrenocortical cancer are insufficient. ► The dual PI3K/mTOR inhibitor NVP-BEZ235 efficiently inhibits ACC cell proliferation. ► Concomitant inhibition of Erk may be required to potentiate the NVP-BEZ235 effect.
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AU-rich elements in the 3′-UTR regulate the stability of the 141 amino acid isoform of parathyroid hormone-related protein mRNAOriginal Research ArticlePages 105-112 Alexander I. Luchin, Murali V.P. Nadella, Nanda K. Thudi, Wessel P. Dirksen, Parul Gulati, Soledad A. Fernandez, Thomas J. Rosol Show preview | Related articles | Related reference work articles
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Highlights
► The instability of PTHrP 1-141 mRNA is determined by four AREs in its 3′-UTR. ► Effects of these AREs are potentially mediated by the tristetraproline (TTP) ARE-binding protein. ► Additional proteins (60–80 kDa) bind specifically to the AREs in HARA cell extracts.
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Cortisol regulates Na+ uptake in zebrafish, Danio rerio, larvae via the glucocorticoid receptorOriginal Research ArticlePages 113-125 Yusuke Kumai, Dinushan Nesan, Mathilakath M. Vijayan, Steve F. Perry Show preview | Related articles | Related reference work articles
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Highlights
► Cortisol stimulates Na+ uptake and ammonia excretion in zebrafish larvae through glucocorticoid receptor. ► The stimulation of Na+ uptake in larvae during acid-exposure is at least partially mediated by increased cortisol level. ► Cortisol stimulates Na+ uptake by stimulating the recently proposed NHE3b–Rhcg1 functional metabolon. ► Glucocorticoid receptor is highly expressed in ionocytes responsible for Na+ uptake.
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Estrogens promote cell–cell adhesion of normal and malignant mammary cells through increased desmosome formationOriginal Research ArticlePages 126-133 Marie Maynadier, Monique Chambon, Ilaria Basile, Michel Gleizes, Philippe Nirde, Magali Gary-Bobo, Marcel Garcia Show preview | Related articles | Related reference work articles
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Highlights
► We proved that estrogens increase cell–cell adhesion in breast cancer cell lines. ► Estrogen increases desmosomes number in normal and breast cancer cells. ► Expression of several desmosomal proteins is increased by estrogen treatment. ► Silencing of the estrogen receptor α expression prevents cell–cell adhesion. ► Silencing of a key desmosomal protein impairs estrogen-induced adhesion.
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