نتایج جستجو برای: proteasome inhibitor

تعداد نتایج: 224881  

Journal: :Acta Crystallographica Section A Foundations and Advances 2014

2015
Kévin Adam Mireille Lambert Elsa Lestang Gabriel Champenois Isabelle Dusanter Jérôme Tamburini Didier Bouscary Catherine Lacombe Yael Zermati Patrick Mayeux

The oncogenic Pim2 kinase is overexpressed in several hematological malignancies such as multiple myeloma and acute myeloid leukemia and constitutes a strong therapeutic target candidate. Like other Pim kinases, Pim2 is constitutively active and is believed to be essentially regulated through its accumulation. We show that in leukemic cells, the three Pim2 isoforms have dramatically short halfl...

Journal: :Chemistry & biology 1998
M Bogyo S Shin J S McMaster H L Ploegh

BACKGROUND The proteasome is a multicatalytic protease complex responsible for most cytosolic protein breakdown. The complex has several distinct proteolytic activities that are defined by the preference of each for the carboxyterminal (P1) amino acid residue. Although mutational studies in yeast have begun to define substrate specificities of individual catalytically active beta subunits, litt...

Journal: :Biochemical pharmacology 2003
Natalia A Osna Dahn L Clemens Terrence M Donohue

We tested the influence of IFNgamma on proteasome activity in parental Hep G2 cells that do not metabolize ethanol, as well as in recombinant Hep G2-derived cells that express either or both alcohol dehydrogenase (ADH) and cytochrome P4502E1 (CYP2E1). IFNgamma treatment increased proteasome activity in VL-17A (ADH(+), CYP2E1(+)) and E-47 (CYP2E1(+)) cells, but not in Hep G2, VI-R2 (parental cel...

Journal: :Circulation 2006
Christophe Depre Qian Wang Lin Yan Nadia Hedhli Pallavi Peter Li Chen Chull Hong Luc Hittinger Bijan Ghaleh Junichi Sadoshima Dorothy E Vatner Stephen F Vatner Kiran Madura

BACKGROUND The adaptation of cardiac mass to hemodynamic overload requires an adaptation of protein turnover, ie, the balance between protein synthesis and degradation. We tested 2 hypotheses: (1) chronic left ventricular hypertrophy (LVH) activates the proteasome system of protein degradation, especially in the myocardium submitted to the highest wall stress, ie, the subendocardium, and (2) th...

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