• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

ADAR1 is essential for the maintenance of hematopoiesis and suppression of interferon signaling.

The deaminase ADAR1 edits adenosines in nuclear transcripts of nervous tissue and is required in the fetal liver of the developing mouse embryo. Here we show by inducible gene disruption in mice that ADAR1 is essential for maintenance of both fetal and adult hematopoietic stem cells. Loss of ADAR1 in hematopoietic stem cells led to global upregulation of type I and II interferon-inducible transcripts and rapid apoptosis. Our findings identify ADAR1 as an essential regulator of hematopoietic stem cell maintenance and suppressor of interferon signaling that may protect organisms from the deleterious effects of interferon activation associated with many pathological processes, including chronic inflammation, autoimmune disorders and cancer.

Pubmed ID: 19060901

Authors

  • Hartner JC
  • Walkley CR
  • Lu J
  • Orkin SH

Journal

Nature immunology

Publication Data

January 17, 2009

Associated Grants

  • Agency: NIDDK NIH HHS, Id: P30 DK049216
  • Agency: NIDDK NIH HHS, Id: P30 DK049216-15
  • Agency: Howard Hughes Medical Institute, Id:
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Adenosine Deaminase
  • Animals
  • Gene Deletion
  • Gene Expression Regulation
  • Hematopoiesis
  • Hematopoietic Stem Cells
  • Inbreeding
  • Interferons
  • Liver
  • Mice
  • Mice, Inbred C57BL
  • RNA-Binding Proteins
  • Signal Transduction