HES1 (human) (rec.) (His)

AdipoGen Life Sciences

HES1 (human) (rec.) (His)

10

Research Use Only

>90%

Transcription factor HES-1

bHLH proteins are essential for neurogenesis, myogenesis, hematopoiesis and sex determination. HES1 (Hairy and Enhancer of Split 1) is a basic Helix-Loop-Helix (bHLH) transcriptional repressor regulated by the Notch pathway and expressed in various tissues. HES1 is well known in development of different tissues, particularly endoderm derived endocrine organs like pancreas and neuroendocrine cells of lung. HES1 controls normal development by regulating proliferation and differentiation and so cell fate. Notch signaling plays both oncogenic and tumor suppressor roles depending on cell type. In contrast to T cell acute lymphoblastic leukemia (ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B cell ALL (B-ALL) leads to growth arrest and apoptosis. The Notch target HES1 is sufficient to reproduce this tumor suppressor phenotype in B-ALL by interacting and activating PARP-1 and regulating proapoptotic signals. - Protein. Human HES1 (aa 2-280) is fused at the N-terminus to a His-tag. Source: E. coli. Liquid. 0.2microm-filtered solution in 55mM TRIS-Cl, pH 8.2, containing 150mM NaCl. Purity: >90% (SDS-PAGE). bHLH proteins are essential for neurogenesis, myogenesis, hematopoiesis and sex determination. HES1 (Hairy and Enhancer of Split 1) is a basic Helix-Loop-Helix (bHLH) transcriptional repressor regulated by the Notch pathway and expressed in various tissues. HES1 is well known in development of different tissues, particularly endoderm derived endocrine organs like pancreas and neuroendocrine cells of lung. HES1 controls normal development by regulating proliferation and differentiation and so cell fate. Notch signaling plays both oncogenic and tumor suppressor roles depending on cell type. In contrast to T cell acute lymphoblastic leukemia (ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B cell ALL (B-ALL) leads to growth arrest and apoptosis. The Notch target HES1 is sufficient to reproduce this tumor suppressor phenotype in B-ALL by interacting and activating PARP-1 and regulating proapoptotic signals.

2°C to 8°C,-20°C

12352202