Our hosting provider will be performing UPS maintenance on Tuesday, Oct 25, 2016 between 8 AM and 5 PM PDT. SciCrunch searching services will be down during this time.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

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

Accelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1.


Dominant RUNX1 inhibition has been proposed as a common pathway for CBF leukemia. CBF beta-SMMHC, a fusion protein in human acute myeloid leukemia (AML), dominantly inhibits RUNX1 largely through its RUNX1 high-affinity binding domain (HABD). However, the type I CBF beta-SMMHC fusion in AML patients lacks HABD. Here, we report that the type I CBF beta-SMMHC protein binds RUNX1 inefficiently. Knockin mice expressing CBF beta-SMMHC with a HABD deletion developed leukemia quickly, even though hematopoietic defects associated with Runx1-inhibition were partially rescued. A larger pool of leukemia-initiating cells, increased MN1 expression, and retention of RUNX1 phosphorylation are potential mechanisms for accelerated leukemia development in these mice. Our data suggest that RUNX1 dominant inhibition may not be a critical step for leukemogenesis by CBF beta-SMMHC.

Pubmed ID: 20478528


  • Kamikubo Y
  • Zhao L
  • Wunderlich M
  • Corpora T
  • Hyde RK
  • Paul TA
  • Kundu M
  • Garrett L
  • Compton S
  • Huang G
  • Wolff L
  • Ito Y
  • Bushweller J
  • Mulloy JC
  • Liu PP


Cancer cell

Publication Data

May 18, 2010

Associated Grants

  • Agency: NCI NIH HHS, Id: CA118319
  • Agency: NCRR NIH HHS, Id: M01 RR 08084
  • Agency: Intramural NIH HHS, Id: Z01 HG000030-13
  • Agency: Intramural NIH HHS, Id: Z01 HG000030-14
  • Agency: Intramural NIH HHS, Id: Z99 HG999999
  • Agency: Intramural NIH HHS, Id: ZIA HG000030-15

Mesh Terms

  • Animals
  • Core Binding Factor Alpha 2 Subunit
  • Core Binding Factor beta Subunit
  • Humans
  • Leukemia, Experimental
  • Mice
  • Mice, Transgenic
  • Oncogene Proteins, Fusion
  • Phosphorylation
  • Protein Binding