Deficiency of β common receptor moderately attenuates the progression of myeloproliferative neoplasm in NrasG12D/+ Mice

Jing Zhang; Jingfang Zhang; Erik A. Ranheim; Juan Du; Yangang Liu; Jinyong Wang; Guangyao Kong

doi:10.1074/jbc.M115.653154

Deficiency of β common receptor moderately attenuates the progression of myeloproliferative neoplasm in Nras^G12D/+ Mice

Jing Zhang
, Jingfang Zhang
, Erik A. Ranheim
, Juan Du
, Yangang Liu
, Jinyong Wang
, Guangyao Kong

University of Wisconsin-Madison

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

Background: GM-CSF signaling is important in establishing and maintaining juvenile/chronic myelomonocytic leukemia (JMML/CMML). Results: The common β chain of GM-CSF receptor (βc) is dispensable for the function of CMML-initiating cells, but βc^-/- prolongs the survival of CMML-bearing mice. Conclusion: βc^-/- slows down CMML progression but does not abrogate its initiation. Significance: Inhibiting GM-CSF signaling might alleviate JMML/CMML symptoms but would not eradicate the disease.

Original language	English
Pages (from-to)	19093-19103
Number of pages	11
Journal	Journal of Biological Chemistry
Volume	290
Issue number	31
DOIs	https://doi.org/10.1074/jbc.M115.653154
State	Published - 31 Jul 2015
Externally published	Yes

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@article{e10770a4009d467daed067870c3ceccc,

title = "Deficiency of β common receptor moderately attenuates the progression of myeloproliferative neoplasm in NrasG12D/+ Mice",

abstract = "Background: GM-CSF signaling is important in establishing and maintaining juvenile/chronic myelomonocytic leukemia (JMML/CMML). Results: The common β chain of GM-CSF receptor (βc) is dispensable for the function of CMML-initiating cells, but βc-/- prolongs the survival of CMML-bearing mice. Conclusion: βc-/- slows down CMML progression but does not abrogate its initiation. Significance: Inhibiting GM-CSF signaling might alleviate JMML/CMML symptoms but would not eradicate the disease.",

author = "Jing Zhang and Jingfang Zhang and Ranheim, \{Erik A.\} and Juan Du and Yangang Liu and Jinyong Wang and Guangyao Kong",

note = "Publisher Copyright: {\textcopyright} 2015 by The American Society for Biochemistry and Molecular Biology, Inc.",

year = "2015",

month = jul,

day = "31",

doi = "10.1074/jbc.M115.653154",

language = "英语",

volume = "290",

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journal = "Journal of Biological Chemistry",

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TY - JOUR

T1 - Deficiency of β common receptor moderately attenuates the progression of myeloproliferative neoplasm in NrasG12D/+ Mice

AU - Zhang, Jing

AU - Zhang, Jingfang

AU - Ranheim, Erik A.

AU - Du, Juan

AU - Liu, Yangang

AU - Wang, Jinyong

AU - Kong, Guangyao

PY - 2015/7/31

Y1 - 2015/7/31

N2 - Background: GM-CSF signaling is important in establishing and maintaining juvenile/chronic myelomonocytic leukemia (JMML/CMML). Results: The common β chain of GM-CSF receptor (βc) is dispensable for the function of CMML-initiating cells, but βc-/- prolongs the survival of CMML-bearing mice. Conclusion: βc-/- slows down CMML progression but does not abrogate its initiation. Significance: Inhibiting GM-CSF signaling might alleviate JMML/CMML symptoms but would not eradicate the disease.

AB - Background: GM-CSF signaling is important in establishing and maintaining juvenile/chronic myelomonocytic leukemia (JMML/CMML). Results: The common β chain of GM-CSF receptor (βc) is dispensable for the function of CMML-initiating cells, but βc-/- prolongs the survival of CMML-bearing mice. Conclusion: βc-/- slows down CMML progression but does not abrogate its initiation. Significance: Inhibiting GM-CSF signaling might alleviate JMML/CMML symptoms but would not eradicate the disease.

UR - https://www.scopus.com/pages/publications/84940489043

U2 - 10.1074/jbc.M115.653154

DO - 10.1074/jbc.M115.653154

M3 - 文章

C2 - 26082490

AN - SCOPUS:84940489043

SN - 0021-9258

VL - 290

SP - 19093

EP - 19103

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 31

ER -

Deficiency of β common receptor moderately attenuates the progression of myeloproliferative neoplasm in Nras^G12D/+ Mice

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