Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Sheo M. Singh"'
Autor:
Wolfgang Hiddemann, Gerhard Behre, Sheo M. Singh, A A PeerZada, A Kieser, Arun Kumar Trivedi, Maximilian Christopeit, D Bararia, Hermann M. Behre
Publikováno v:
Oncogene 26, 1789-1801 (2007)
Functional inactivation of transcription factors in hematopoietic stem cell development is involved in the pathogenesis of acute myeloid leukemia (AML). Stem cell regulator C/enhancer binding protein (EBP)alpha is among such transcription factors kno
Autor:
Hanna S. Radomska, Gerhard Behre, Sheo M. Singh, Laura T. Bortolin, Daniel G. Tenen, Janki Rangatia, Max Christopeit, Huaitian Liu, Alan D. Friedman, Wolfgang Hiddemann
Publikováno v:
Journal of Biological Chemistry. 277:26293-26299
The transcription factor C/EBP alpha regulates early steps of normal granulocyte differentiation since mice with a disruption of the C/EBP alpha gene do not express detectable levels of the granulocyte colony-stimulating factor receptor and produce n
Autor:
Arun Kumar Trivedi, Sabyasachi Sanyal, Sheo M. Singh, Jitendra Kumar Kanaujiya, Gerhard Behre, Pooja Pal, Maximilian Christopeit, Savita Lochab
Publikováno v:
Electrophoresis. 32(3-4)
After human genome is decoded, the characterization of the proteins is the next challenging task. The study of the complete protein complement of the genome, the 'proteome' referred to as proteomics, is an important tool for the identification of new
Publikováno v:
Biochemical and biophysical research communications. 369(2)
Phosphorylation of C/EBPalpha can either lead to granulocytic differentiation or a block in granulopoiesis. This dichotomy in effect is dependent on the upstream signaling pathway and the phosphorylation site in C/EBPalpha. Ras signaling induced phos
Publikováno v:
European journal of cancer (Oxford, England : 1990). 44(11)
Transcription factors play a crucial role in myeloid differentiation and lineage determination. Tumour suppressor protein C/EBPalpha is a key regulator of granulocytic differentiation whose functional inactivation has become a pathophysiological sign
Autor:
Alexander Kohlmann, Annika Elsässer, Abdul A Peer Zada, Wolfgang Hiddemann, Gerhard Behre, Torsten Haferlach, Daniel G. Tenen, Sheo M. Singh, Janki Rangatia, Rajani Kanth Vangala
Publikováno v:
Oncogene. 22(30)
Transcription factor C/EBPalpha induces normal myeloid differentiation, inactivation of C/EBPalpha leads to a differentiation block in acute myeloid leukemias (AML), and overexpression of C/EBPalpha results in AML growth arrest and differentiation. R
Autor:
Torsten Haferlach, Daniel G. Tenen, Venkateshwar A Reddy, Abdul A Peer Zada, Gerhard Behre, Annika Elsässer, Alexander Meisel, Sheo M. Singh, Wolfgang Hiddemann
Publikováno v:
Oncogene. 22(15)
In the present study, we investigated the mechanism of CD44 ligation with the anti-CD44 monoclonal antibody A3D8 to inhibit the proliferation of human acute myeloid leukemia (AML) cells. The effects of A3D8 on myeloid cells were associated with speci
Autor:
Wolfgang Hiddemann, Claudia Schoch, Gerhard Behre, Daniel G. Tenen, Marion S. Heiss-Neumann, Sheo M. Singh, Janki Rangatia, Rajani Kanth Vangala
Publikováno v:
Blood. 101(1)
The transcription factor PU.1 plays a pivotal role in normal myeloid differentiation. PU.1−/− mice exhibit a complete block in myeloid differentiation. Heterozygous PU.1 mutations were reported in some patients with acute myeloid leukemia (AML),
Autor:
Gerhard Behre, Abdul A Peer Zada, Sheo M. Singh, Daniel G. Tenen, Venkateshwar A Reddy, Wolfgang Hiddemann
Publikováno v:
Expert opinion on therapeutic targets. 6(4)
Recent results indicate that interactions of transcription factors with other nuclear proteins play an important role in stem cell development, lineage commitment and differentiation in the haematopoietic system, and the pathogenesis of myeloid leuka
Autor:
Maximilian Christopeit, Arun Kumar Trivedi, Savita Lochab, Sheo M. Singh, Gerhard Behre, Wolfgang Hiddemann
Publikováno v:
Clinical Proteomics. 6(3):83-91
Introduction The rational design of targeted therapies for acute myeloid leukemia (AML) requires the discovery of novel protein pathways in the systems biology of a specific AML subtype. We have shown that in the AML subtype with translocation t(8;21