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101.
The angiotensin II type I (AT(1)) receptor mediates regulation of blood pressure and water-electrolyte balance by Ang II. Substitution of Gly for Asn(111) of the AT(1) receptor constitutively activates the receptor leading to Gq-coupled IP(3) production independent of Ang II binding. The Ang II-activated conformation of the AT1(N111G) receptor was proposed to be similar to that of the wild-type AT(1) receptor, although, various aspects of the Ang II-induced conformation of this constitutively active mutant receptor have not been systematically studied. Here, we provide evidence that the conformation of the active state of the wild-type and the constitutively active AT(1) receptors are different. Upon Ang II binding an activated conformation of the wild-type AT(1) receptor activates G protein and recruits beta-arrestin. In contrast, the agonist-bound AT1(N111G) mutant receptor preferentially couples to Gq and is inadequate in beta-arrestin recruitment. 相似文献
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In this study, based on the view of statistical inference, we investigate the robustness of neural codes, i.e., the sensitivity
of neural responses to noise, and its implication on the construction of neural coding. We first identify the key factors
that influence the sensitivity of neural responses, and find that the overlap between neural receptive fields plays a critical
role. We then construct a robust coding scheme, which enforces the neural responses not only to encode external inputs well,
but also to have small variability. Based on this scheme, we find that the optimal basis functions for encoding natural images
resemble the receptive fields of simple cells in the striate cortex. We also apply this scheme to identify the important features
in the representation of face images and Chinese characters.
相似文献
Sheng LiEmail: |
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Si Zhang Zhongnan Yin Fei-Fei Dai Hao Wang Meng-Jiao Zhou Ming-Hui Yang Shu-Feng Zhang Zhi-Feng Fu Ying-Wu Mei Ming-Xi Zang Lixiang Xue 《Journal of cellular physiology》2019,234(8):13252-13262
Although cardiac hypertrophy is widely recognized as a risk factor that leads to cardiac dysfunction and, ultimately, heart failure, the complex mechanisms underlying cardiac hypertrophy remain incompletely characterized. The nuclear receptor peroxisome proliferator-activated receptor δ (PPARδ) is involved in the regulation of cardiac lipid metabolism. Here, we describe a novel PPARδ-dependent molecular cascade involving microRNA-29a (miR-29a) and atrial natriuretic factor (ANF), which is reactivated in cardiac hypertrophy. In addition, we identify a novel role of miR-29a, in which it has a cardioprotective function in isoproterenol hydrochloride-induced cardiac hypertrophy by targeting PPARδ and downregulating ANF. Finally, we provide evidence that miR-29a reduces the isoproterenol hydrochloride-induced cardiac hypertrophy response, thereby underlining the potential clinical relevance of miR-29a in which it may serve as a potent therapeutic target for heart hypertrophy treatment. 相似文献