PMID- 25941081
OWN - NLM
STAT- MEDLINE
DCOM- 20161221
LR  - 20181113
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 778
DP  - 2016 May 5
TI  - Signal transduction and chemotaxis in mast cells.
PG  - 11-23
LID - S0014-2999(15)00397-0 [pii]
LID - 10.1016/j.ejphar.2015.02.057 [doi]
AB  - Mast cells play crucial roles in both innate and adaptive arms of the immune 
      system. Along with basophils, mast cells are essential effector cells for 
      allergic inflammation that causes asthma, allergic rhinitis, food allergy and 
      atopic dermatitis. Mast cells are usually increased in inflammatory sites of 
      allergy and, upon activation, release various chemical, lipid, peptide and 
      protein mediators of allergic reactions. Since antigen/immunoglobulin E 
      (IgE)-mediated activation of these cells is a central event to trigger allergic 
      reactions, innumerable studies have been conducted on how these cells are 
      activated through cross-linking of the high-affinity IgE receptor (FcepsilonRI). 
      Development of mature mast cells from their progenitor cells is under the 
      influence of several growth factors, of which the stem cell factor (SCF) seems to 
      be the most important. Therefore, how SCF induces mast cell development and 
      activation via its receptor, KIT, has been studied extensively, including a 
      cross-talk between KIT and FcepsilonRI signaling pathways. Although our understanding 
      of the signaling mechanisms of the FcepsilonRI and KIT pathways is far from complete, 
      pharmaceutical applications of the knowledge about these pathways are underway. 
      This review will focus on recent progresses in FcepsilonRI and KIT signaling and 
      chemotaxis.
CI  - Copyright (c) 2015 Elsevier B.V. All rights reserved.
FAU - Draber, Petr
AU  - Draber P
AD  - Department of Signal Transduction, Institute of Molecular Genetics, Academy of 
      Sciences of the Czech Republic, CZ 14220 Prague, Czech Republic. Electronic 
      address: petr.draber@img.cas.cz.
FAU - Halova, Ivana
AU  - Halova I
AD  - Department of Signal Transduction, Institute of Molecular Genetics, Academy of 
      Sciences of the Czech Republic, CZ 14220 Prague, Czech Republic.
FAU - Polakovicova, Iva
AU  - Polakovicova I
AD  - Department of Signal Transduction, Institute of Molecular Genetics, Academy of 
      Sciences of the Czech Republic, CZ 14220 Prague, Czech Republic.
FAU - Kawakami, Toshiaki
AU  - Kawakami T
AD  - Division of Cell Biology, La Jolla Institute for Allergy and Immunology, 9420 
      Athena Circle La Jolla, CA 92037, USA; Laboratory for Allergic Disease, RIKEN 
      Center for Integrative Medical Sciences (IMS-RCAI), Yokohama 230-0045, Japan.
LA  - eng
GR  - R01 AR064418/AR/NIAMS NIH HHS/United States
GR  - R01 HL124283/HL/NHLBI NIH HHS/United States
GR  - 1R01HL124283-01/HL/NHLBI NIH HHS/United States
GR  - R01 AR064418-01A1/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150502
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
SB  - IM
MH  - Animals
MH  - *Chemotaxis/drug effects
MH  - Humans
MH  - Mast Cells/*cytology/drug effects
MH  - *Signal Transduction/drug effects
PMC - PMC4630209
MID - NIHMS686928
OTO - NOTNLM
OT  - Chemotaxis
OT  - IgE receptor
OT  - KIT receptor
OT  - Mast cell
OT  - Plasma membrane
OT  - Signal transduction
EDAT- 2015/05/06 06:00
MHDA- 2016/12/22 06:00
PMCR- 2017/05/05
CRDT- 2015/05/06 06:00
PHST- 2014/11/25 00:00 [received]
PHST- 2015/02/09 00:00 [revised]
PHST- 2015/02/17 00:00 [accepted]
PHST- 2015/05/06 06:00 [entrez]
PHST- 2015/05/06 06:00 [pubmed]
PHST- 2016/12/22 06:00 [medline]
PHST- 2017/05/05 00:00 [pmc-release]
AID - S0014-2999(15)00397-0 [pii]
AID - 10.1016/j.ejphar.2015.02.057 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2016 May 5;778:11-23. doi: 10.1016/j.ejphar.2015.02.057. Epub 
      2015 May 2.