نتایج جستجو برای: ucp2

تعداد نتایج: 918  

2011
Rodolfo Niño Fong Zahra Fatehi-Hassanabad Simon C Lee Hongfang Lu Michael B Wheeler Catherine B Chan

Mutations in the uncoupling protein 2 (Ucp2) gene are linked to type-2 diabetes. Here, a potential mechanism by which lack of UCP2 is cytoprotective in pancreatic β-cells was investigated. Nitric oxide (NO) production was elevated in Ucp2(-/-) islets. Proliferation (cyclin D2, Ccnd2) and anti-apoptosis (Tnfaip3) genes had increased expression in Ucp2(-/-) islets, whereas the mRNA of pro-apoptos...

Journal: :FEBS letters 1998
M V Carretero L Torres U Latasa E R García-Trevijano J Prieto J M Mato M A Avila

Uncoupling protein 2 (UCP2) expression in liver is restricted to non-parenchymal cells. By means of differential display screening between normal rat liver and H4IIE hepatoma cells we have isolated a cDNA clone encompassing part of UCP2 cDNA. Northern blot analysis revealed that UCP2 is expressed in some hepatocarcinoma cell lines, while it is absent in adult hepatocytes. UCP2 mRNA in H4IIE cel...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2007
Yalin Emre Corinne Hurtaud Melis Karaca Tobias Nubel Flora Zavala Daniel Ricquier

Infiltration of inflammatory cells into pancreatic islets of Langerhans and selective destruction of insulin-secreting beta-cells are characteristics of type 1 diabetes. Uncoupling protein 2 (UCP2) is a mitochondrial protein expressed in immune cells. UCP2 controls macrophage activation by modulating the production of mitochondrial reactive oxygen species (ROS) and MAPK signaling. We investigat...

ژورنال: :physiology and pharmacology 0
fatemeh safari yazd cardiovascular research center, shahid sadoughi university of medical sciences, yazd, iran غلامرضا بیات gholamreza bayat dept. of physiology and pharmacology, alborz university of medical sciences, karaj, iran شهناز شکرفروش shahnaz shekarforoush dept. of physiology, islamic azad university, arsanjan branch, fars, iran عاصفه فکری asefeh fekri yazd cardiovascular research center, shahid sadoughi university of medical sciences, yazd, iran سید حسین مشتاقیون seyyed hosein moshtaghioun yazd cardiovascular research center, shahid sadoughi university of medical sciences, yazd, iran مهدی فروزنده مقدم mahdi foruzande moghadam dept. of biotechnology, tarbiat modares university, tehran, iran سهراب حاجی‏زاده

مقدمه: تجمع رادیکالهای آزاد اکسیژن (ros) از مهمترین مکانیسم های مسؤول ایجاد آسیب های ناشی از ایسکمی- رپرفیوژن میوکارد است. مطالعات نشان می دهد که پروتئین ucp2 توسط ros فعال شده و به طور فیدبکی تولید ros را کاهش می دهد. هدف از این مطالعه بررسی اثر ایسکمی- رپرفیوژن میوکارد بر سطح mrna و پروتئین ucp2 در قلب موش صحرایی می باشد . روش ها: در این مطالعه از موش های صحرایی نر نژاد ویستار (250 تا 300 گرم...

2015
Suho Lee Hyunji Moon Gayoung Kim Jeong Hoon Cho Lee Dae-Hee Michael B. Ye Daeho Park

Rapid and efficient engulfment of apoptotic cells is an essential property of phagocytes for removal of the large number of apoptotic cells generated in multicellular organisms. To achieve this, phagocytes need to be able to continuously uptake apoptotic cells. It was recently reported that uncoupling protein 2 (Ucp2) promotes engulfment of apoptotic cells by increasing the phagocytic capacity,...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2002
Takako Kizaki Kenji Suzuki Yoshiaki Hitomi Naoyuki Taniguchi Daizoh Saitoh Kenji Watanabe Kazunori Onoé Noorbibi K Day Robert A Good Hideki Ohno

The expression of uncoupling protein 2 (UCP2) was reduced in macrophages after stimulation with lipopolysaccharide (LPS). The physiological consequence and the regulatory mechanisms of the UCP2 down-regulation by LPS were investigated in a macrophage cell line, RAW264 cells. UCP2 overexpression in RAW264 cells transfected with eukaryotic expression vector containing ucp2 cDNA markedly reduced t...

Journal: :The Journal of clinical endocrinology and metabolism 1998
P Barbe L Millet D Larrouy J Galitzky M Berlan J P Louvet D Langin

Uncoupling protein-2 (UCP2) is a mitochondrial protein expressed in a wide range of human tissues. By uncoupling respiration from ATP synthesis, UCP2 might be involved in the control of energy expenditure. We have investigated UCP2 gene expression in human adipose tissue. In eight subjects, we found a positive correlation (r = 0.91, P < 0.002) between subcutaneous and visceral fat depots UCP2 m...

Journal: :Circulation 2003
J Blanc M C Alves-Guerra B Esposito S Rousset P Gourdy D Ricquier A Tedgui B Miroux Z Mallat

BACKGROUND Uncoupling protein 2 (UCP2) regulates the production of reactive oxygen species in macrophages. However, its role in atherosclerosis is unknown. METHODS AND RESULTS Irradiated low-density lipoprotein receptor deficient mice (LDLR-/-) were transplanted with bone marrow from either UCP2 deficient mice (Ucp2-/-) or wild type mice (Ucp2+/+). Mice were fed an atherogenic diet for 7 week...

Journal: :Cell 2001
Chen-Yu Zhang György Baffy Pascale Perret Stefan Krauss Odile Peroni Danica Grujic Thilo Hagen Antonio J. Vidal-Puig Olivier Boss Young-Bum Kim Xin Xiao Zheng Michael B. Wheeler Gerald I. Shulman Catherine B. Chan Bradford B. Lowell

beta cells sense glucose through its metabolism and the resulting increase in ATP, which subsequently stimulates insulin secretion. Uncoupling protein-2 (UCP2) mediates mitochondrial proton leak, decreasing ATP production. In the present study, we assessed UCP2's role in regulating insulin secretion. UCP2-deficient mice had higher islet ATP levels and increased glucose-stimulated insulin secret...

2016
Ren-Hong Du Fang-Fang Wu Ming Lu Xiao-dong Shu Jian-Hua Ding Guangyu Wu Gang Hu

Mitochondrial uncoupling protein 2 (UCP2) has been well characterized to control the production of reactive oxygen species (ROS) and astrocytes are the major cells responsible for the ROS production and the inflammatory responses in the brain. However, the function of UCP2 in astrocytes and the contribution of astrocytic UCP2 to depression remain undefined. Herein, we demonstrated that UCP2 kno...

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