Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Mar 12;9:481. doi: 10.3389/fimmu.2018.00481

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2018 Hasan, Naqvi and Rizvi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Impact of HOXA10 on acute myeloid leukemia (AML) development and emergency granulopoiesis (EG) through regulation of myelopoiesis. HOXA10 overexpression in murine bone marrow leads to enhanced myeloproliferation, which progresses into AML through acquisition of additional mutations and differentiation block. HOXA10 effects EG by regulating the gene ARIH2, which encodes TRIAD1, a ubiquitin ligase. In vitro stimulation of myeloid progenitors with granulocyte colony stimulating factor (G-CSF) showed HOXA10-dependent increase in TRIAD1 expression. Increased TRIAD1 expression degrades fibroblast growth factor receptor-1 (FGFR1), reduces the effect of FGF2, and terminates the effect of FGF2 on myeloid progenitor expansion. As G-CSF is the main mediator of EG, these processes result in termination of EG with HOXA10 being the prime regulator. Suppressed EG response during infections in leukemic conditions may serve as one of the causes of neutropenia.