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IFNB1 — MYD88
Pathways - manually collected, often from reviews:
-
KEGG Tuberculosis:
MYD88
→
IFNB1
(gene expression, expression)
Text-mined interactions from Literome
Schilling et al., J Immunol 2002
:
TLR4 dependent induction of IL-6 expression did require Toll-IL-1R domain containing adapter protein ( TIRAP )
/MyD88 adapter-like (Mal) , but unlike iNOS and IP-10, it did not
require the expression of
IFN-beta
Yamamoto et al., J Immunol 2002
:
Furthermore, TRIF, but neither
MyD88 nor TIRAP,
activated the
IFN-beta promoter
Oshiumi et al., J Biol Chem 2003
:
Although MyD88 and Mal/TIRAP adapters functions downstream of TLR4, DC maturation and
IFN-beta induction are
independent of
MyD88 and Mal/TIRAP
Sugiyama et al., Microbiol Immunol 2004
:
These results suggested that 2-AP
inhibited LPS induced
IFN-beta production by preventing Toll/IL-1 receptor domain containing adaptor inducing IFN-beta ( TRIF ) -dependent signaling rather than
myeloid differentiation factor (MyD) 88-dependent signaling, resulting in the inhibition of NO production
Hirotani et al., Biochem Biophys Res Commun 2005
:
Regulation of lipopolysaccharide-inducible genes by
MyD88 and Toll/IL-1 domain containing adaptor
inducing IFN-beta
Toshchakov et al., J Immunol 2005
(MAP Kinase Signaling System) :
We designed a set of `` blocking peptides '' ( BPs ) comprised of the 14 aa that correspond to the sequences of the BB loops of the four known Toll-IL-1 resistance ( TIR ) domain containing adapter proteins ( i.e.,
MyD88 , TIR domain containing adapter
inducing IFN-beta ( TRIF ), TRIF related adapter molecule (TRAM), and TIR-domain containing adapter protein ( TIRAP ) ) linked to the cell penetrating segment of the antennapedia homeodomain
Zhang et al., J Immunol 2009
(Multiple Sclerosis, Relapsing-Remitting) :
Using small interfering RNA TLR7 gene silencing, we confirmed that
IFN-beta1a induced changes in
MyD88 , IL-1R associated kinase 4, and IL-1R expression were dependent on TLR7
Siegemund et al., J Virol 2009
:
iPPVO elicits IFN-alpha/beta by Toll-like receptor ( TLR ) -independent pathways in BM-cDC, since
IFN-alpha/beta release does not
require myeloid differentiation primary response gene 88 (
MyD88 ) or TIR-domain containing adaptor protein inducing interferon ( TRIF )
Burns et al., J Immunol 2010
(Bacteroidaceae Infections) :
Proinflammatory cytokine production in response to P. gingivalis infection depends on TLR2, but it does not require
MyD88 or TLR/IL-1R-domain containing adaptor
inducing IFN-beta
Tam et al., Immunology 2009
(Listeriosis) :
Together the data suggest an inhibitory effect of IFN-alpha/beta on functional DC maturation during Listeria infection and reveal overlapping roles of
MyD88 induced cytokines and
IFN-alpha/beta in DC maturation and protective anti-Listeria immunity
Prantner et al., J Immunol 2010
:
Previous studies have demonstrated no role for TLR4 and a partial
role for
MyD88 in chlamydial induced
IFN-beta
Liu et al., J Immunol 2010
:
Zebrafish
Myd88 alone strongly
induced the activation of NF-kappaB and
IFN-beta both in HEK293T and carp leukocyte cells
Gratz et al., PLoS Pathog 2011
(Cellulitis) :
Macrophages required IRF3, STING, TBK1 and partially MyD88, whereas in cDCs the
IFN-beta production was fully
dependent on IRF5 and
MyD88