نتایج جستجو برای: nuclear hypertrophy

تعداد نتایج: 279538  

Journal: :Development 2011
John J McCarthy Jyothi Mula Mitsunori Miyazaki Rod Erfani Kelcye Garrison Amreen B Farooqui Ratchakrit Srikuea Benjamin A Lawson Barry Grimes Charles Keller Gary Van Zant Kenneth S Campbell Karyn A Esser Esther E Dupont-Versteegden Charlotte A Peterson

An important unresolved question in skeletal muscle plasticity is whether satellite cells are necessary for muscle fiber hypertrophy. To address this issue, a novel mouse strain (Pax7-DTA) was created which enabled the conditional ablation of >90% of satellite cells in mature skeletal muscle following tamoxifen administration. To test the hypothesis that satellite cells are necessary for skelet...

Journal: :Circulation research 2009
Wei Liu Min Zi Jiawei Jin Sukhpal Prehar Delvac Oceandy Tomomi E Kimura Ming Lei Ludwig Neyses Arthur H Weston Elizabeth J Cartwright Xin Wang

Mitogen-activated protein kinase kinase (MKK)4 is a critical member of the mitogen-activated protein kinase family. It is able to activate the c-Jun NH(2)-terminal protein kinase (JNK) and p38 mitogen-activated protein kinase in response to environmental stresses. JNK and p38 are strongly implicated in pathological cardiac hypertrophy and heart failure; however, the regulatory mechanism whereby...

Journal: :The Journal of biological chemistry 2006
Erik W Bush David B Hood Philip J Papst Joseph A Chapo Wayne Minobe Michael R Bristow Eric N Olson Timothy A McKinsey

The calcium/calmodulin-dependent phosphatase calcineurin plays a central role in the control of cardiomyocyte hypertrophy in response to pathological stimuli. Although calcineurin is present at high levels in normal heart, its activity appears to be unaffected by calcium during the course of a cardiac cycle. The mechanism(s) whereby calcineurin is selectively activated by calcium under patholog...

Journal: :The Biochemical journal 2011
Jaya P Gangopadhyay Noriaki Ikemoto

We have shown previously that the inter-domain interaction between the two domains of RyR (ryanodine receptor), CaMBD [CaM (calmodulin)-binding domain] and CaMLD (CaM-like domain), activates the Ca(2+) channel, and this process is called activation-link formation [Gangopadhyay and Ikemoto (2008) Biochem. J. 411, 415-423]. Thus CaM that is bound to CaMBD is expected to interfere the activation-l...

Journal: :American journal of physiology. Heart and circulatory physiology 2013
Vinodkumar B Pillai Nagalingam R Sundaresan Gene Kim Sadhana Samant Liliana Moreno-Vinasco Joe G N Garcia Mahesh P Gupta

Nicotinamide phosphoribosyltransferase (Nampt) is an important coenzyme involved in cellular redox reactions. Inside the cell, Nampt (iNampt) functions as a rate-limiting enzyme in the NAD salvage pathway, and outside the cell (eNampt), it acts as a proinflammatory cytokine. High-circulating levels of Nampt are reported in different pathological conditions. This study was designed to examine th...

Journal: :Circulation research 2010
Hideyuki Kinoshita Koichiro Kuwahara Motohiro Nishida Zhong Jian Xianglu Rong Shigeki Kiyonaka Yoshihiro Kuwabara Hitoshi Kurose Ryuji Inoue Yasuo Mori Yuhao Li Yasuaki Nakagawa Satoru Usami Masataka Fujiwara Yuko Yamada Takeya Minami Kenji Ueshima Kazuwa Nakao

RATIONALE Atrial and brain natriuretic peptides (ANP and BNP, respectively) exert antihypertrophic effects in the heart via their common receptor, guanylyl cyclase (GC)-A, which catalyzes the synthesis of cGMP, leading to activation of protein kinase (PK)G. Still, much of the network of molecular mediators via which ANP/BNP-GC-A signaling inhibit cardiac hypertrophy remains to be characterized....

2017
Feby Savira Longxing Cao Ian Wang Wendi Yang Kevin Huang Yue Hua Beat M Jucker Robert N Willette Li Huang Henry Krum Zhiliang Li Qiang Fu Bing Hui Wang

Intracellular accumulation of protein-bound uremic toxins in the setting of cardiorenal syndrome leads to adverse effects on cardiorenal cellular functions, where cardiac hypertrophy and cardiorenal fibrosis are the hallmarks. In this study, we sought to determine if Apoptosis Signal-Regulated Kinase 1 (ASK1), an upstream regulator of cellular stress response, mediates cardiac hypertrophy and c...

Journal: :Ophthalmic surgery, lasers & imaging : the official journal of the International Society for Imaging in the Eye 2010
Gabriella De Salvo Ilse Krebs Susanne Binder

The authors describe the use of high-definition optical coherence tomography (HD-OCT) in a case of congenital hypertrophy of the retinal pigment epithelium. A 40-year-old woman presented with a large flat pigmented lesion in the inferior retinal quadrant of the left eye, which was compatible with congenital hypertrophy of the retinal pigment epithelium. The lesion was studied with HD-OCT (5 lin...

Journal: :Circulation research 2014
Yoon Seok Nam Yoojung Kim Hosouk Joung Duk-Hwa Kwon Nakwon Choe Hyun-Ki Min Yong Sook Kim Hyung-Seok Kim Don-Kyu Kim Young Kuk Cho Yong-Hoon Kim Kwang-Il Nam Hyoung Chul Choi Dong Ho Park Kyoungho Suk In-Kyu Lee Youngkeun Ahn Chul-Ho Lee Hueng-Sik Choi Gwang Hyeon Eom Hyun Kook

RATIONALE Small heterodimer partner (SHP; NR0B2) is an atypical orphan nuclear receptor that lacks a conventional DNA-binding domain. Through interactions with other transcription factors, SHP regulates diverse biological events, including glucose metabolism in liver. However, the role of SHP in adult heart diseases has not yet been demonstrated. OBJECTIVE We aimed to investigate the role of ...

Journal: :The Journal of biological chemistry 2005
Esther Latres Ami R Amini Ashley A Amini Jennifer Griffiths Francis J Martin Yi Wei Hsin Chieh Lin George D Yancopoulos David J Glass

Skeletal muscle size is regulated by anabolic (hypertrophic) and catabolic (atrophic) processes. We first characterized molecular markers of both hypertrophy and atrophy and identified a small subset of genes that are inversely regulated in these two settings (e.g. up-regulated by an inducer of hypertrophy, insulin-like growth factor-1 (IGF-1), and down-regulated by a mediator of atrophy, dexam...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید