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Specialty: Endocrinology
Cancer: Retinoblastoma

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Total 5 results found since Jan 2013.

PLAC8 is overexpressed and regulates cell proliferation in low-grade human PanNET
Conclusion: Our findings establish PLAC8 as a central mediator of cell growth in a subset of human PanNET, providing evidence for the existence of distinct molecular subtypes within this class of tumors.
Source: Neuroendocrinology - April 25, 2019 Category: Endocrinology Source Type: research

Involvement of the STAT5-CyclinD/CDK4-pRb pathway in beta cell proliferation stimulated by prolactin during pregnancy.
Abstract During pregnancy, maternal pancreatic beta cells undergo a compensatory expansion in response to the state of insulin resistance, where prolactin (PRL) plays a major role. Retinoblastoma protein (Rb) has been shown to critically regulate islet proliferation and function. The aim of the study was to explore the role of Rb in beta cell mass expansion during pregnancy. During pregnancy, expression of Rb, phospho-Rb (p-Rb), p107 and E2F1 increased, while p130 decreased in maternal islets. With PRL stimulation, induction of Rb expression occurred mainly in the nucleus while p-Rb was predominantly in the cytopl...
Source: Am J Physiol Endocri... - December 4, 2018 Category: Endocrinology Authors: Zhao X, Xu Y, Wu Y, Zhang H, Shi H, Zhu H, Woo M, Wu X Tags: Am J Physiol Endocrinol Metab Source Type: research

Molecular cloning, expression pattern analysis of porcine Rb1 gene and its regulatory roles during primary dedifferentiated fat cells adipogenic differentiation.
Abstract Adipocytes are the main constituent of adipose tissue and are considered to be a corner stone in the homeostatic control of whole body metabolism. Recent reports evidenced that retinoblastoma 1 (Rb1) gene plays an important role in fat development and adipogenesis in mice. Here, we cloned the partial cDNA sequences of the porcine Rb1 gene which contains the complete coding sequences (CDS) of 2820bp encoding a protein of 939 amino acids. Bioinformatic analysis revealed that the CDS of porcine Rb1 was highly identical with those of cattle, human and mice. The porcine Rb1 has three typical conserved structur...
Source: General and Comparative Endocrinology - January 24, 2015 Category: Endocrinology Authors: Hu X, Luo P, Peng X, Song T, Zhou Y, Wei H, Peng J, Jiang S Tags: Gen Comp Endocrinol Source Type: research

Differential Signaling by Regulatory Subunits of Phosphoinositide-3-kinase Influences Cell Survival in INS-1E Insulinoma Cells
In conclusion, signalling of p50α, p55α and p85α is similar at the level of Akt, but differentially influence downstream GSK-3 activation and cell cycle entry. PI3K isoform p50α induction by cytokines provides a link between regeneration and cell survival under cytotoxic stress in insulin-producing pancreatic beta-cells.[...]© Georg Thieme Verlag KG Stuttgart · New YorkArticle in Thieme eJournals:Table of contents  |  Abstract  |  Full text
Source: Experimental and Clinical Endocrinology and Diabetes - November 13, 2014 Category: Endocrinology Authors: Schrader, J.Niebel, P.Rossi, A.Archontidou-Aprin, E.Hörsch, D. Tags: Article Source Type: research

GPER mediates the inhibitory actions of estrogen on adipogenesis in 3T3-L1 cells through perturbation of mitotic clonal expansion.
Abstract G-protein-coupled estrogen receptor 1 (GPER) mediates non-genomic signaling of estrogenic events. Here we showed for the first time that Gper/GPER is expressed in Swiss 3T3 mouse embryo preadipocytes 3T3-L1, and that Gper/GPER is up-regulated during differentiation of the cells induced by monocyte differentiation-inducing (MDI) cocktail. Activation of GPER by the natural ligand 17β-estradiol (E2), and the specific agonist G1, was shown to inhibit lipid accumulation in 3T3-L1 cells, while such inhibition was reversed upon knockdown of GPER using specific siRNA. GPER was also found to mediate perturbation ...
Source: General and Comparative Endocrinology - July 17, 2013 Category: Endocrinology Authors: Zhu P, Yuen JM, Sham KW, Cheng CH Tags: Gen Comp Endocrinol Source Type: research