MIR155

Antisense RNA MIR155

Maps_Modules
MODULE:INPUT_INHIBITORS MODULE:IMMUNE_SUPPRESSION MODULE:IMMUNOSUPPRESSIVE_CYTOKINE_PATHWAYS MODULE:INPUT_ACTIVATORS MODULE:TUMOR_RECOGNTITON MODULE:NK_ACTIVATING_RECEPTORS MODULE:CORE_SIGNALING_PATHWAYS MODULE:MIRNA_TF_IMMUNOSTIMULATORY

References
NATURAL_KILLER
MACROPHAGE
CASCADE:IL10
CASCADE:IL4
CASCADE:IL13
CASCADE:KLRB1
PMID:24227772
KLRB1 (NK1.1) ligation also induce MIR155 expression
PMID:23422749
The enhanced NK-cell survival, expansion, activation, and tumor control result from overexpression of miR-155 in NK cells.
PMID:19359473, PMID:22378844, PMID:24227772
Inositol phosphatase SHIP1 is a primary and direct target of miR-155.
miR-155 upregulates IFNG production in natural killer cells via SHIP1 downregulation.
Inhibition of either calcineurin or PI3Kled to a dose-responsive decrease in the differential between 155−/− and WT NK cell
But an the same time mRNAs targeted by miR-155 were enriched in NK cell activation signaling pathways.
SLP76, IKBKE mRNA are MIR55 targets.
PMID:23572582
NOXA , a proapoptotic Bcl-2 homology domain (BH3)-only protein, is an important regulator of survival in NK cells
ans SOCS1 are mir155 targets in NK cells
PMID:21097505
miR-155 Directly Targets IL13RA1, reduces the IL-13- and IL-4-dependent Phosphorylation of STAT6 in Human Macrophages and downregulates IL-13 dependent GENES
PMID:21385848
miR155 induction is required for efficient DC maturation and is critical for the ability of DCs to promote antigen-specific T-cell activation.
miR155 expression was increased strongly in mature Mo-DCs relative to monocytes and immature Mo-DCs.

Modifications:
In compartment: INNATE_IMMUNE_CELL_Cytosol

arMIR155@INNATE_IMMUNE_CELL_Cytosol

Participates in complexes:
In compartment: INNATE_IMMUNE_CELL_Cytosol

Participates in reactions:
As Reactant or Product:

As Catalyser: