Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas

Carly Leung, Merel E Lingbeek, +5 authors Silvia Marino
Published 2004 in Nature

Abstract

Overexpression of the polycomb group gene Bmi1 promotes cell proliferation and induces leukaemia through repression of Cdkn2a (also known as ink4a/Arf) tumour suppressors. Conversely, loss of Bmi1 leads to haematological defects and severe progressive neurological abnormalities in which de-repression of the ink4a/Arf locus is critically implicated. Here, we… (More)

DOI: 10.1038/nature02385

J. M. Ruppert, B. Vogelstein, K. W. Kinzler
Mol . Cell
2003

Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas

Abstract

4 Figures and Tables

Topics

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References

A Molecular Fingerprint for Medulloblastoma 1

Bmi - 1 regulation of INK 4 A - ARF is a downstream requirement for transformation of hematopoietic progenitors by E 2 a - Pbx 1

Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation

Bmi-1 determines the proliferative capacity of normal and leukaemic stem cells

Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells

Nmyc upregulation by sonic hedgehog signaling promotes proliferation in developing cerebellar granule neuron precursors.

Targeting mTOR signaling for cancer therapy.

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

Dissecting p53 tumor suppressor functions in vivo.

Global and specific translational control by rapamycin in T cells uncovered by microarrays and proteomics.

Presentations referencing similar topics

Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas

Abstract

4 Figures and Tables

Topics

Cited By

The function of E 2 F 6 in the Polycomb complex by

GSK3β Regulates Differentiation and Growth Arrest in Glioblastoma

The biology of cancer stem cells.

Heterozygous knockout of the Bmi-1 gene causes an early onset of phenotypes associated with brain aging

Acute myeloid leukemia with t(10;17)(p13;q12) chromosome translocation: a case report and literature review.

Bmi1 marks intermediate precursors during differentiation of human brain tumor initiating cells.

Epigenetic principles and mechanisms underlying nervous system functions in health and disease.

Stem cells use distinct self-renewal programs at different ages.

The Mechanisms of Hedgehog Signal Transduction

Id1 and Sonic Hedgehog Mediate Cell Cycle Reentry and Apoptosis Induced by Amyloid Beta-Peptide in Post-mitotic Cortical Neurons

References

A Molecular Fingerprint for Medulloblastoma 1

Bmi - 1 regulation of INK 4 A - ARF is a downstream requirement for transformation of hematopoietic progenitors by E 2 a - Pbx 1

Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation

Bmi-1 determines the proliferative capacity of normal and leukaemic stem cells

Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells

Nmyc upregulation by sonic hedgehog signaling promotes proliferation in developing cerebellar granule neuron precursors.

Targeting mTOR signaling for cancer therapy.

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

Dissecting p53 tumor suppressor functions in vivo.

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