Charakterisierung und Regulation des humanen mad1-Promotors
type: CreativeWork
description: The transcriptionfactor Mad1 is a potential tumorsuppressor. As a member of the Myc/Max/Madnetwork it antagonizes the transforming ability of the protooncogene c-myc. It was shown, that Mad1 can inhibit the transformation of REFs by c-myc/Ras through blockade of the G1/S-transition. Moreover it was shown, that Mad1 is an inhibitor of apoptosis. The members of the Myc/Max/Madnetwork are transcriptonfactors and regulate gene-expression after binding to specific DNA-sequences and then recruiting chromatin-modifying factors. In principle c-myc is described as an activator of transcription while mad1 is described as an inhibitor of transcription. Mad1 is an essential factor in the development of myeloid cells and loss of Mad1-function results in delayed differentiation of granulocytes and monocytes. Accordingly to this it fits, that mad1 gets upregulated after TPA- or GCSF-stimulation of U937-cells. Therefore it is interesting to know how Mad1 itself is transcriptionally regulated, to get more insight into crucial cellular processes like proliferation and differentiation. What are essential extracellular factors and what different intracellular signaltransduction-pathways are involved? In this study a human DNA-fragment was isolated which has mad1-promoter-function and contains a set of regulatory elements like binding sites for transcriptionfactors. This promoter-fragment is located only a few basepairs upstream of the translation-start-site. Alignement of this human sequence with DNA-sequences of mouse and rat reveales a box with nearly 70% homology and binding sites for transcriptionfactors important for myeloid development and differentiation. The mad1-promoter is very GC-rich and contains no TATA-box. In this study one transcription-start-site of the mad1-gene was identified. It is located at the 3´-end of the homologous promoter region. The influence of chromatin and its modifications on transcription is known. So it is important to investigate the nucleosomal stru…
abstract: The transcriptionfactor Mad1 is a potential tumorsuppressor. As a member of the Myc/Max/Madnetwork it antagonizes the transforming ability of the protooncogene c-myc. It was shown, that Mad1 can inhibit the transformation of REFs by c-myc/Ras through blockade of the G1/S-transition. Moreover it was shown, that Mad1 is an inhibitor of apoptosis. The members of the Myc/Max/Madnetwork are transcriptonfactors and regulate gene-expression after binding to specific DNA-sequences and then recruiting chromatin-modifying factors. In principle c-myc is described as an activator of transcription while mad1 is described as an inhibitor of transcription. Mad1 is an essential factor in the development of myeloid cells and loss of Mad1-function results in delayed differentiation of granulocytes and monocytes. Accordingly to this it fits, that mad1 gets upregulated after TPA- or GCSF-stimulation of U937-cells. Therefore it is interesting to know how Mad1 itself is transcriptionally regulated, to get more insight into crucial cellular processes like proliferation and differentiation. What are essential extracellular factors and what different intracellular signaltransduction-pathways are involved? In this study a human DNA-fragment was isolated which has mad1-promoter-function and contains a set of regulatory elements like binding sites for transcriptionfactors. This promoter-fragment is located only a few basepairs upstream of the translation-start-site. Alignement of this human sequence with DNA-sequences of mouse and rat reveales a box with nearly 70% homology and binding sites for transcriptionfactors important for myeloid development and differentiation. The mad1-promoter is very GC-rich and contains no TATA-box. In this study one transcription-start-site of the mad1-gene was identified. It is located at the 3´-end of the homologous promoter region. The influence of chromatin and its modifications on transcription is known. So it is important to investigate the nucleosomal stru…
author: Eckert, Kolja
language: ger
keywords: info:eu-repo/classification/ddc/610, Medizin, Transkription, Chromatin, Nukleosomen, Hämatopoese, GCSF/R, Signaltransduktion
date published: 2005
date modified: 2026-07-30T19:42:48Z
provider: RWTH Aachen University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Publikationsserver der RWTH Aachen University