The Role of ERα and ERβ in theProstate: Insights from Genetic Models and Isoform-Selective Ligands

2007 ◽  
pp. 131-148 ◽  
Author(s):  
S. J. McPherson ◽  
S. J. Ellem ◽  
V. Patchev ◽  
K. H. Fritzemeier ◽  
G. P. Risbridger
Keyword(s):  
Genetic Models ◽  
Selective Ligands

scholarly journals Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis

Diabetologia ◽  
2016 ◽  
Vol 59 (5) ◽  
pp. 1012-1020 ◽  
Author(s):  
Joan Mir-Coll ◽  
Jordi Duran ◽  
Felipe Slebe ◽  
Mar García-Rocha ◽  
Ramon Gomis ◽  
...  
Keyword(s):  
Beta Cell ◽  
Glucose Homeostasis ◽  
Genetic Models ◽  
Rule Out

Deciphering the specific role of Gαi/o isoforms: functional selective oxytocin ligands and somatostatin SST5 receptor mutants

2013 ◽  
Vol 41 (1) ◽  
pp. 166-171 ◽  
Author(s):  
Marta Busnelli ◽  
Erika Peverelli ◽  
Giovanna Mantovani ◽  
Anna Spada ◽  
Bice Chini
Keyword(s):  
Somatostatin Receptor ◽  
Receptor Activation ◽  
G Protein Coupled Receptors ◽  
Receptor Coupling ◽  
Biological Responses ◽  
Selective Ligands ◽  
Specific Effector ◽  
G Protein Coupled

Receptor coupling to different G-proteins and β-arrestins has been described for a number of GPCRs (G-protein-coupled receptors), suggesting a multi-state model of receptor activation in which each receptor can assume a number of different active conformations, each capable of promoting the coupling to a specific effector. Consistently, functional-selective ligands and biased agonists have been described to be able to induce and/or stabilize only a subset of specific active conformations. Furthermore, GPCR mutants deficient in selective coupling have been reported. Functional selective ligands and receptor mutants thus constitute unique tools to dissect the specific roles of different effectors, in particular among the Gi/o family. In the present mini-review, we focus on (i) the identification of functional selective OXT (oxytocin)-derived peptides capable of activating single Gi/o isoforms, namely Gi1 or Gi3; and (ii) the characterization of an SS (somatostatin) receptor SST5 mutant selectively impaired in its GoA coupling. These analogues and receptor mutants represent unique tools for examining the contribution of Gi/o isoforms in complex biological responses and open the way for the development of drugs with peculiar selectivity profiles.

scholarly journals Current Developments on the Role of α1-Adrenergic Receptors in Cognition, Cardioprotection, and Metabolism

2021 ◽  
Vol 9 ◽  
Author(s):  
Dianne M. Perez
Keyword(s):  
Adrenergic Receptors ◽  
Smooth Muscle Contraction ◽  
The Body ◽  
Whole Body ◽  
Selective Ligands ◽  
Recent Developments ◽  
Vascular Smooth Muscle Contraction ◽  
G Protein Coupled ◽  
Similar Affinity

The α1-adrenergic receptors (ARs) are G-protein coupled receptors that bind the endogenous catecholamines, norepinephrine, and epinephrine. They play a key role in the regulation of the sympathetic nervous system along with β and α2-AR family members. While all of the adrenergic receptors bind with similar affinity to the catecholamines, they can regulate different physiologies and pathophysiologies in the body because they couple to different G-proteins and signal transduction pathways, commonly in opposition to one another. While α1-AR subtypes (α1A, α1B, α1C) have long been known to be primary regulators of vascular smooth muscle contraction, blood pressure, and cardiac hypertrophy, their role in neurotransmission, improving cognition, protecting the heart during ischemia and failure, and regulating whole body and organ metabolism are not well known and are more recent developments. These advancements have been made possible through the development of transgenic and knockout mouse models and more selective ligands to advance their research. Here, we will review the recent literature to provide new insights into these physiological functions and possible use as a therapeutic target.

scholarly journals MBOAT7-TMC4 rs641738 Is Not Associated With the Risk of Hepatocellular Carcinoma or Persistent Hepatitis B Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Peng Wang ◽  
Ying Li ◽  
Lu Li ◽  
Rong Zhong ◽  
Na Shen
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B ◽  
Meta Analysis ◽  
Hbv Infection ◽  
Genetic Models ◽  
Transmembrane Channel ◽  
B Virus ◽  
Membrane Bound ◽  
Control Study

ObjectiveA hot genetic variant, rs641738 within the membrane-bound O-acyltransferase domain containing 7(MBOAT7) and transmembrane channel-like 4 (TMC4), was recently reported to be associated with several liver diseases. However, the results remain controversial. Therefore, this study aimed to explore the role of MBOAT7-TMC4 rs641738 in the risk of hepatocellular carcinoma (HCC) and persistent hepatitis B virus (HBV) infection.MethodsWe first conducted a case-control study that included 779 HCC cases and 1412 cancer-free controls. Controls consisted of 678 persistent HBV carriers and 734 spontaneously recovered subjects. The gene variant rs641738 was genotyped using the MassARRAY platform. The results were analyzed in five genetic models using multivariate logistic regression analyses. Next, we performed a systematic review and meta-analysis to further explore the role of this variant in HCC risk.ResultsThe results suggested no association between MBOAT7-TMC4 rs641738 and HCC risk in most genetic models (all P > 0.05). Although a marginally significant association was observed in TT vs. CC (P = 0.037) and the recessive models (P = 0.044). The meta-analysis of 2135 HCC cases and 4388 controls supported that this variant was not related to HCC risk, even in the TT vs. CC and recessive models. We also determined that this variant did not influence persistent HBV infection.ConclusionOur work highlights that MBOAT7-TMC4 rs641738 is not associated with the risk of HCC or persistent HBV infection. This study provides some clues to identify the “truth” of potential disease-related genetic factors in the post-genome era.

scholarly journals Homocysteine metabolism in rodent models with hyperhomocysteinemia. Part 1: genetic models

2020 ◽  
pp. 118-124
Author(s):  
А.В. Иванов ◽  
Э.Д. Вирюс ◽  
В.И. Логинов ◽  
И.С. Зимина ◽  
А.М. Бурдённый ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Kidney Failure ◽  
Genetic Models ◽  
Rodent Models ◽  
Rats And Mice

Моделирование гипергомоцистеинемии на грызунах является одним из основных способов изучения роли гомоцистеина в патофизиологии различных заболеваний (инфаркта миокарда, инсультов, когнитивных нарушений, болезни Альцгеймера, почечной недостаточности и др.). В настоящем обзоре рассмотрены биохимичекие аспекты метаболизма гомоцистеина, генетические способы моделирования гипергомоцистеинемии на крысах и мышах и их влияние на метаболизм как самого гомоцистеина так и на связанные с ним метаболиты: метионин, цистеин, S-аденозилметионин, S-аденозилгомоцистеин. Modeling hyperhomocysteinemia in rodents is a common way to study the role of homocysteine in pathogenesis of various diseases (myocardial infarction, stroke, cognitive impairment, Alzheimer’s disease, kidney failure, etc.). This review focuses on biochemical aspects of homocysteine metabolism, genetic methods for modeling hyperhomocysteinemia in rats and mice, and effects of these models on metabolism of both homocysteine itself and related metabolites (methionine, cysteine, S-adenosylmethionine, S-adenosylhomocysteine).

The Role of NOS in Heart Failure: Lessons from Murine Genetic Models

2006 ◽  
pp. 113-128 ◽  
Author(s):  
Imran N. Mungrue ◽  
Mansoor Husain ◽  
Duncan J. Stewart
Keyword(s):  
Heart Failure ◽  
Genetic Models

One Gene vs. Two Genes in Schizophrenia

1974 ◽  
Vol 125 (587) ◽  
pp. 348-349 ◽  
Author(s):  
Carol Buck
Keyword(s):  
Single Gene ◽  
Genetic Models ◽  
Intermediate Model ◽  
Genetic Mechanisms

Arguments about the role of heredity in schizophrenia have largely given way to arguments about the genetic mechanisms involved. Discussions of the various genetic models by leading workers in the field have been presented in recent years (Rosenthal and Kety, 1968; Kaplan, 1972). Single gene theories have prevailed, Slater's intermediate model being preferred because of its good fit with the observed risks of schizophrenia in specific categories of blood relatives (Slater and Cowie, 1971).

scholarly journals Endothelium-derived ET-1 and the development of renal injury

2015 ◽  
Vol 309 (9) ◽  
pp. R1071-R1073 ◽  
Author(s):  
Carmen De Miguel ◽  
David M. Pollock ◽  
Jennifer S. Pollock
Keyword(s):  
Renal Injury ◽  
Genetic Models ◽  
Endothelin 1 ◽  
Working Hypothesis ◽  
Renal Tubular ◽  
Vasoactive Peptide

The role of the vasoactive peptide endothelin-1 (ET-1) in renal injury is not fully understood. In this review, we examine the genetic models available to understand the autocrine/paracrine mechanisms by which ET-1 leads to renal injury and propose the working hypothesis that endothelium-derived ET-1 induces renal injury by initiating renal tubular apoptosis in a paracrine manner.

Rethinking genetic models of asthma: the role of environmental modifiers

2005 ◽  
Vol 17 (6) ◽  
pp. 670-678 ◽  
Author(s):  
Carole Ober ◽  
Emma E Thompson
Keyword(s):  
Genetic Models
Sign in / Sign up

Export Citation Format

Share Document