SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation.
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Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn's Disease-Like Ileitis: What is the Right Model?Analysis of the human monocyte-derived macrophage transcriptome and response to lipopolysaccharide provides new insights into genetic aetiology of inflammatory bowel disease.SHIP-1 Couples to the Dectin-1 hemITAM and Selectively Modulates Reactive Oxygen Species Production in Dendritic Cells in Response to Candida albicansDendritic-cell expression of Ship1 regulates Th2 immunity to helminth infection in mice.Analysis of SHIP1 expression and activity in Crohn's disease patientsLyn prevents aberrant inflammatory responses to infection in mammalian systems by repressing a SHIP-1-associated signaling cluster
P2860
SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation.
description
2014 nî lūn-bûn
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name
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@en
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@nl
type
label
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@en
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@nl
prefLabel
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@en
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@nl
P2093
P2860
P356
P1433
P1476
SHIP-1 deficiency in the myelo ...... nsion or chronic inflammation.
@en
P2093
E Tsantikos
M J Maxwell
N Srivastava
R W Engelman
P2860
P2888
P304
P356
10.1038/GENE.2014.9
P577
2014-03-06T00:00:00Z