This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Neurogenetics  • Neurology, Other  • Review  • Alert me on articles by topic  Social Bookmarking   What's this?

Paul S. Knoepfler, PhD

Arch Neurol. 2008;65(3):311-315.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Mutations that cause autosomal recessive primary microcephaly (MCPH), including MCPH1 through MCPH6, have provided insight into the normal programming that directs brain growth and defines ultimate brain size. The common denominator in these mutations is that they all manifest within neural stem and progenitor cells, decreasing their numbers at various stages of neurogenesis. Microcephalin (MCHP1) and abnormal spindlelike, microcephaly associated (MCPH5) have been the focus of most of the research. However, the recent discovery of microcephaly caused by mutation of the N-myc (also MYCN) proto-oncogene both in mice, where it was directed specifically to neural stem cells, and in the germ line in humans in Feingold syndrome has shed new light on the role of neural stem cells in brain growth. N-myc controls brain growth not only by regulating neural stem cell proliferation, but also through maintaining a . . . [Full Text of this Article]

CHROMATIN ON THE BRAIN: MCHP1

MCPH2 THROUGH MCPH6 AND CHROMOSOME DYNAMICS

Myc ON THE BRAIN

A CHROMATIN CONNECTION?

FUTURE DIRECTIONS

AUTHOR INFORMATION

Author Affiliation: Department of Cell Biology and Human Anatomy, Institute of Pediatric Regenerative Medicine, Shriners Hospital for Children Northern California, University of California Davis School of Medicine, Sacramento.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?