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6 documents found
1: Title: Oncogenic acidic nuclear phosphoproteins ANP32C/D are novel clients of heat shock protein 90.
Authors: Yuzefovych, Yuliia, et.al. .
Journal: Biochimica et biophysica acta (Biochim Biophys Acta), Vol. 1853 (10 Pt A): 2338-48, 2015 .
Snippet: Further studies treating cells with the Hsp90 inhibitors PU-H71 and 17-AAG showed atypical increased protein stability and prevention of ANP32C degradation compared to the Hsp90 client AKT.
Affiliation: Institute for Transfusion Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. Institute for Transfusion Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. Electronic address: huyton.trevor@mh-hannover.de. .
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2: Title: Cracking the ANP32 whips: important functions, unequal requirement, and hints at disease implications.
Authors: Reilly, Patrick T, et.al. .
Journal: BioEssays : news and reviews in molecular, cellular and developmental biology (Bioessays), Vol. 36 (11): 1062-71, 2014 .
Snippet: We also present hypotheses that ANP32C and other intronless sequences should not currently be considered bona fide family members, that their disparate necessity in development may be due to compensatory mechanisms, that their contrasting roles in cancer are likely context-dependent, along with an underlying hypothesis that ANP32s represent an important node of physiological regulation by virtue of their diverse biochemical activities.
Affiliation: Laboratory of Inflammation Biology, National Cancer Centre Singapore, Singapore, Singapore. .
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3: Title: pp32r1 controls the decay of the RNA-binding protein HuR.
Authors: Imamachi, Kenji, et.al. .
Journal: Oncology reports (Oncol Rep), Vol. 31 (3): 1103-8, 2014 .
Snippet: Even with lethal stress such as staurosporine (STS), HuR in the cytoplasm was never downregulated, and caspase-3 activity was inhibited when cells expressed pp32r1.
Affiliation: Department of Oral Pathology and Biology, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan. Department of Oral and Maxillofacial Surgery, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan. Department of Oral Diagnosis and Medicine, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan. .
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4: Title: Overexpression of the pp32r1 (ANP32C) oncogene or its functional mutant pp32r1Y140H confers enhanced resistance to FTY720 (Finguimod).
Authors: Buddaseth, Salma, et.al. .
Journal: Cancer biology & therapy (Cancer Biol Ther), Vol. 15 (3): 289-96, 2014 .
Snippet: pp32r1 (ANP32C) is oncogenic and has been shown to be overexpressed in tumors of the breast, prostate, and pancreas.
Affiliation: Institute for Transfusion Medicine; Hannover Medical School; Hannover, Germany. .
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5: Title: Dysregulation of cell cycle control caused by overexpression of the oncogene pp32r1 (ANP32C) and the Tyr>His mutant pp32r1Y140H.
Authors: Buddaseth, Salma, et.al. .
Journal: Biochimica et biophysica acta (Biochim Biophys Acta), Vol. 1833 (5): 1212-21, 2013 .
Snippet: The pp32 (ANP32A) gene acts as a tumor suppressor while its closely related homologue pp32r1 (ANP32C) is oncogenic and is overexpressed in breast, prostate and pancreatic tumors.
Affiliation: Institute for Transfusion Medicine, Hannover Medical School, Hannover, Germany. .
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6: Title: Identification of a functional mutation in pp32r1 (ANP32C).
Authors: Kochevar, G John, et.al. .
Journal: Human mutation (Hum Mutat), Vol. 23 (6): 546-51, 2004 .
Snippet: No mutations or polymorphisms have previously been reported in pp32r1 (ANP32C; GenBank: AF008216.1).
Affiliation: Department of Pathology, Texas A&M University System Health Science Center, College Station, Texas, USA. .
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