Ignet

Gene Information

Gene symbol: MIRN146A

Gene name: microRNA 146a

HGNC ID: 31533

Related Genes

#	Gene Symbol	Number of hits
1	DUSP1	1 hits
2	IFNG	1 hits
3	IL6	1 hits
4	IRAK1	1 hits
5	JUN	1 hits
6	MAPK1	1 hits
7	MAPK14	1 hits
8	MIRN125A	1 hits
9	MIRN132	1 hits
10	MIRN155	1 hits
11	MIRN196A2	1 hits
12	MIRN29A	1 hits
13	RBM4	1 hits
14	TLR4	1 hits
15	TNF	1 hits
16	TRAF6	1 hits

Related Sentences

#	PMID	Sentence
1	19819280	Critical parameters for assessment of the optimal functional state of DCs and prediction of the vaccine potency of activated DCs have in the past been based on measurements of differentiation surface markers like HLA-DR, CD80, CD83, CD86, and CCR7 and the level of secreted cytokines like interleukin-12p70.
2	19819280	Of these, four miRNAs, hsa-miR-155, hsa-miR-146a, hsa-miR-125a-5p, and hsa-miR-29a, were validated by real-time polymerase chain reaction and northern blotting.
3	20434553	Splenocytes were separated for detection of lymphocyte proliferation in responses to concanavalin A (Con A), lipopolysaccharide (LPS) and OVA, and mRNA expression of Th1 cytokines (IFN-gamma and IL-12), Th2 cytokines (IL-10 and IL-5) and transcription factors T-bet/GATA-3 (Th1/Th2 switcher).
4	20434553	In addition, up-regulated T-bet/GATA-3 together with significantly increased mRNA expression of IL-4, IL-10, IFN-gamma and IL-12 by splenocytes, as well as the proliferative responses of splenocytes to Con A, LPS and OVA were observed in paclitaxel-adjuvanted groups.
5	20434553	Incubation of a murine macrophage-like cell line with paclitaxel significantly increased TNF-alpha and -10 released from the cells and expression of microRNAs such as miR-155, miR-147, miR-146a and miR-132.
6	23807362	To investigate whether selected single nucleotide polymorphisms (SNPs) in miR-146a, miR-196a2, miR-27a, miR-26a-1, miR-124 and miR-149 genes are associated with immune response to hepatitis B vaccine.
7	23825193	We previously reported that sepsis differentially represses transcription and translation of tumor necrosis factor alpha (TNF-α) and interleukin 1β (IL-1β) to reprogram sepsis inflammation.
8	23825193	We showed that phosphorylation-dependent activation of p38 mitogen-activated protein kinase (MAPK) and translation disruption of TNF-α and IL-6 follow increased MAPK phosphatase 1 (MKP-1) expression and that MKP-1 knockdown rephosphorylates p38 and restores the capacity to translate TNF-α and IL-6 mRNAs.
9	23825193	We also observed that the RNA-binding protein motif 4 (RBM4), a p38 MAPK target, accumulates in an unphosphorylated form in the cytosol in endotoxin-adapted cells, suggesting that dephosphorylated RBM4 may function as a translational repressor.
10	23825193	Moreover, MKP-1 knockdown promotes RBM4 phosphorylation, blocks its transfer from the nucleus to the cytosol, and reverses translation repression.
11	23825193	We also found that microRNA 146a (miR-146a) knockdown prevents and miR-146a transfection induces MKP-1 expression, which lead to increases or decreases in TNF-α and IL-6 translation, respectively.
12	23825193	We conclude that a TLR4-, miR-146a-, p38 MAPK-, and MKP-1-dependent autoregulatory pathway regulates the translation of proinflammatory genes during the acute inflammatory response by spatially and temporally modifying the phosphorylation state of RBM4 translational repressor protein.
13	23825193	We previously reported that sepsis differentially represses transcription and translation of tumor necrosis factor alpha (TNF-α) and interleukin 1β (IL-1β) to reprogram sepsis inflammation.
14	23825193	We showed that phosphorylation-dependent activation of p38 mitogen-activated protein kinase (MAPK) and translation disruption of TNF-α and IL-6 follow increased MAPK phosphatase 1 (MKP-1) expression and that MKP-1 knockdown rephosphorylates p38 and restores the capacity to translate TNF-α and IL-6 mRNAs.
15	23825193	We also observed that the RNA-binding protein motif 4 (RBM4), a p38 MAPK target, accumulates in an unphosphorylated form in the cytosol in endotoxin-adapted cells, suggesting that dephosphorylated RBM4 may function as a translational repressor.
16	23825193	Moreover, MKP-1 knockdown promotes RBM4 phosphorylation, blocks its transfer from the nucleus to the cytosol, and reverses translation repression.
17	23825193	We also found that microRNA 146a (miR-146a) knockdown prevents and miR-146a transfection induces MKP-1 expression, which lead to increases or decreases in TNF-α and IL-6 translation, respectively.
18	23825193	We conclude that a TLR4-, miR-146a-, p38 MAPK-, and MKP-1-dependent autoregulatory pathway regulates the translation of proinflammatory genes during the acute inflammatory response by spatially and temporally modifying the phosphorylation state of RBM4 translational repressor protein.
19	24561744	EV71 infection upregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon production.
20	24561744	We further identify AP1 as being responsible for the EV71-induced expression of miR-146a.
21	24561744	Surprisingly, knocking out miR-146a or neutralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augments IFNβ production, inhibits viral propagation and improves survival in the mouse model.
22	24561744	Our results suggest that enterovirus-induced miR-146a facilitates viral pathogenesis by suppressing IFN production and provide a clue to developing preventive and therapeutic strategies for enterovirus infections.
23	24561744	EV71 infection upregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon production.
24	24561744	We further identify AP1 as being responsible for the EV71-induced expression of miR-146a.
25	24561744	Surprisingly, knocking out miR-146a or neutralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augments IFNβ production, inhibits viral propagation and improves survival in the mouse model.
26	24561744	Our results suggest that enterovirus-induced miR-146a facilitates viral pathogenesis by suppressing IFN production and provide a clue to developing preventive and therapeutic strategies for enterovirus infections.
27	24561744	EV71 infection upregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon production.
28	24561744	We further identify AP1 as being responsible for the EV71-induced expression of miR-146a.
29	24561744	Surprisingly, knocking out miR-146a or neutralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augments IFNβ production, inhibits viral propagation and improves survival in the mouse model.
30	24561744	Our results suggest that enterovirus-induced miR-146a facilitates viral pathogenesis by suppressing IFN production and provide a clue to developing preventive and therapeutic strategies for enterovirus infections.
31	24561744	EV71 infection upregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon production.
32	24561744	We further identify AP1 as being responsible for the EV71-induced expression of miR-146a.
33	24561744	Surprisingly, knocking out miR-146a or neutralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augments IFNβ production, inhibits viral propagation and improves survival in the mouse model.
34	24561744	Our results suggest that enterovirus-induced miR-146a facilitates viral pathogenesis by suppressing IFN production and provide a clue to developing preventive and therapeutic strategies for enterovirus infections.