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Gene Information

Gene symbol: IRF8

Gene name: interferon regulatory factor 8

HGNC ID: 5358

Synonyms: IRF-8, ICSBP

Related Genes

# Gene Symbol Number of hits
1 BCR 1 hits
2 CYBB 1 hits
3 IFNG 1 hits
4 IFNGR1 1 hits
5 IFNGR2 1 hits
6 IKBKG 1 hits
7 IL12B 1 hits
8 IL12RB1 1 hits
9 IRF1 1 hits
10 IRF4 1 hits
11 ISG15 1 hits
12 MYD88 1 hits
13 STAT1 1 hits
14 TBX21 1 hits
15 TLR9 1 hits

Related Sentences

# PMID Sentence
1 17313486 Sequence analysis for potentially candidate genes such as IRF8, MyD88, TLR9, T-bet were performed.
2 17313486 Flow cytometric analysis showed that almost all patient's peripheral B cells had the transitional phenotype (CD24(bright) CD38(bright) CD27(neg)).
3 17313486 Sequence analysis for TLR9, MyD88, IRF8 and T-bet showed no mutations.
4 17313486 Sequence analysis for potentially candidate genes such as IRF8, MyD88, TLR9, T-bet were performed.
5 17313486 Flow cytometric analysis showed that almost all patient's peripheral B cells had the transitional phenotype (CD24(bright) CD38(bright) CD27(neg)).
6 17313486 Sequence analysis for TLR9, MyD88, IRF8 and T-bet showed no mutations.
7 19171873 Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
8 19171873 Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
9 19171873 We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.
10 19171873 Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.
11 19171873 Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
12 19171873 Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
13 19171873 We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.
14 19171873 Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.
15 23817430 Francisella tularensis SchuS4 and SchuS4 lipids inhibit IL-12p40 in primary human dendritic cells by inhibition of IRF1 and IRF8.
16 25453225 Since 1996, nine MSMD-causing genes, including seven autosomal (IFNGR1, IFNGR2, STAT1, IL12B, IL12RB1, ISG15, and IRF8) and two X-linked (NEMO, and CYBB) genes have been discovered.
17 25453225 These disorders impair the production of (IL12B, IL12RB1, IRF8, ISG15, NEMO) or the response to (IFNGR1, IFNGR2, STAT1, IRF8, CYBB) IFN-γ.
18 25453225 Since 1996, nine MSMD-causing genes, including seven autosomal (IFNGR1, IFNGR2, STAT1, IL12B, IL12RB1, ISG15, and IRF8) and two X-linked (NEMO, and CYBB) genes have been discovered.
19 25453225 These disorders impair the production of (IL12B, IL12RB1, IRF8, ISG15, NEMO) or the response to (IFNGR1, IFNGR2, STAT1, IRF8, CYBB) IFN-γ.
20 25658110 Although, Ara-LAM modulates TLR2 and MAPK signaling, it is not known whether Ara-LAM involves IFN-γ signaling for effective parasite clearance.
21 25658110 Moreover, Ara-LAM reciprocally modulates IRF4 and IRF8 expression and reinstates anti-leishmanial Th1 response that eventuates in significantly reduced parasite load in spleen and liver of L. donovani-infected BALB/c mice.
22 25719445 Further analyses showed that VLP protection requires the transcription factor, IRF8 known to amplify type I IFN signaling in dendritic cells and macrophages, the probable sites of initial EBOV infection.