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IL2 — JUN
Pathways - manually collected, often from reviews:
-
BioCarta the 41bb-dependent immune response:
c-JUN (JUN)
→
IL-2 (IL2)
(transcription, collaborate)
-
NCI Pathway Database Calcineurin-regulated NFAT-dependent transcription in lymphocytes:
JUN/NFAT1-c-4/p21SNFT complex (JUN-NFATC1_NFATC2_NFATC3-BATF3)
→
IL2 (IL2)
(transcription, inhibits)
Iacobelli et al., J Immunol 2000
Evidence: reporter gene
-
NCI Pathway Database Calcium signaling in the CD4+ TCR pathway:
JUN/NFAT1-c-4/p21SNFT complex (JUN-NFATC1_NFATC2_NFATC3-BATF3)
→
IL2 (IL2)
(transcription, inhibits)
Iacobelli et al., J Immunol 2000, Jain et al., J Immunol 1992, Jain et al., Nature 1993
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Calcineurin-regulated NFAT-dependent transcription in lymphocytes:
JUN/FOS/NFAT1-c-4 complex (FOS-JUN-NFATC1_NFATC2_NFATC3)
→
IL2 (IL2)
(transcription, activates)
Safford et al., Nat Immunol 2005
Evidence: mutant phenotype
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Kobata et al., Nihon rinsho. Japanese journal of clinical medicine 1999
:
Consequently, Ras/MAP kinase and PLC gamma 1 pathways are activated to
induce IL-2 gene transcription through
AP-1 and NF-AT generation
Iacobelli et al., J Immunol 1999
:
Similarly,
IL-2 neither activates JNK nor
increases AP-1 binding activity to a consensus o-tetradecanoylphorbol 13-acetate ( TPA ) response element
Zhang et al., J Immunol 1999
:
T cell proliferation and production of
IL-2 , IL-4, and IFN-gamma
induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the
c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580
Mortellaro et al., J Immunol 1999
:
New immunosuppressive drug PNU156804 blocks
IL-2 dependent proliferation and NF-kappa B and
AP-1 activation
Seppänen et al., Oncol Res 1998
(Adenocarcinoma...) :
In the present study, we have investigated the
effects of interferons-alpha (IFN-alpha) and -gamma ( IFN-gamma ),
interleukin-10 (IL-10) and -13 ( IL-13 ), transforming growth factor-beta1 ( TGF-beta1 ), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and induction of transcription factors
AP-1 and NF-kappaB in UM-EC-3 human endometrial adenocarcinoma cells and UT-OC-5 ovarian carcinoma cells in vitro
Yea et al., J Pharmacol Exp Ther 2000
(Thymoma) :
Role of nuclear factor of activated T-cells and
activator protein-1 in the inhibition of
interleukin-2 gene transcription by cannabinol in EL4 T-cells
Wang et al., J Neuroimmunol 2000
:
The neuropeptides VIP and PACAP
inhibit IL-2 transcription by decreasing
c-Jun and increasing JunB expression in T cells
Yan et al., Biochem Biophys Res Commun 2000
:
However,
IL-2 induced
activator protein-1 (AP-1) is oxidation-sensitive ... Gel shift assays of nuclear extracts immunodepleted of Ref-1 protein demonstrated that
IL-2 induced
AP-1 DNA binding is dependent on the presence of Ref-1
Okuma et al., Jpn J Pharmacol 2001
:
The findings suggest that M1 muscarinic receptors are involved in muscarinic receptor mediated enhancement of
IL-2 production in Jurkat cells and that the transcription factor
AP-1 and pathways via mitogen activated protein kinase ( MAPK ) /extracellular signal regulated protein kinase and c-Jun N-terminal kinase, but not via p38 MAPK, may be
involved in the muscarinic receptor mediated enhancement of IL-2 production
García-Lora et al., Cancer Immunol Immunother 2001
:
Here we report that PSK
enhanced AP-1 and CRE binding activities, whereas
IL-2 increased AP-1 and SP-1 and modified GAS/ISRE, IRF-1 and STAT5
Liacini et al., Matrix Biol 2002
(Osteoarthritis, Hip) :
Inhibition of
interleukin-1 stimulated MAP kinases,
activating protein-1 (AP-1) and nuclear factor kappa B (NF-kappa B) transcription factors down-regulates matrix metalloproteinase gene expression in articular chondrocytes
Kim et al., EMBO J 2002
:
Thus, our data indicate an important
role for both
AP-1 and NFAT proteins for TCR induced
IL-2Ralpha expression and establish that both upstream and intronic sequences mediate TCR responsiveness of the IL-2Ralpha gene
Luo et al., Chin Med J (Engl) 2002
:
Decreased
IL-2 expression is, at least in part,
due to a decline in the activation of NFAT and
AP-1 in traumatized mice
Ponti et al., Eur J Immunol 2002
:
Our results show that IL-2 activates CREB in human NK cells and that CREB activation hasa prominent regulatory role on the
IL-2 induced expression of functional c-fos and
AP-1 in NK cells
Zhou et al., Toxicological sciences : an official journal of the Society of Toxicology 2003
:
In this study we show by electrophoretic mobility-shift assay ( EMSA ) that enriched splenic NK cells from EtOH consuming C57BL/6 mice exhibit reduced NF-kappaB and
AP-1 binding activity in
response to
IL-2 stimulation as compared to the water drinking mice
Faubert Kaplan et al., Int Immunopharmacol 2003
:
This decrease in
IL-2 was
due to inhibition of
activator protein-1 (AP-1) and nuclear factor of activated T cells ( NF-AT ) transcription factors, both of which depend on proteins that are regulated by the extracellular signal regulated kinase subgroup of the mitogen activated protein kinases ( ERK MAPK )
Oukka et al., J Exp Med 2004
:
KRC physically associates with the c-Jun transcription factor and serves as a coactivator to augment
AP-1 dependent
IL-2 gene transcription
Yun et al., Toxicology 2006
:
These results suggest that PhIP has potential immunosuppressive effects by inhibiting T-cell proliferation and
IL-2 expression through down regulation of ROS generation and thereby
inhibiting NF-kappaB,
AP-1 and NF-AT activation
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating Toll-like receptor ( TLR )
-interleukin 1 receptor (IL-1R) signaling and subsequent
activation of NF-kappaB and
AP-1 , transcriptional activators of innate immunity
Hayashi et al., J Immunol 2006
:
Depletion of FLNa by RNA interference did not affect TCR induced early tyrosine phosphorylation or actin polymerization but, nevertheless, resulted in impaired
IL-2 expression by human primary T cells and reduced
activation of NF-kappaB,
AP-1 , and NFAT reporter genes in transfected T cells
Duré et al., Mol Immunol 2009
:
Interestingly, we also show that this effect is likely due to changes on the levels of
AP-1 activation
induced by
IL-2 receptor signaling in T cells
Shen et al., Curr Eye Res 2009
:
Under high glucose conditions,
interleukin-1beta significantly
increased expression of
c-Jun and decreased the expression of glutamine synthetase
Nguyen et al., Mol Immunol 2010
:
NFAT and
AP-1 proteins
induce interleukin-2 (IL-2) transcription in stimulated T cells, but the contributions of individual members of these activator families to synergistically activating IL-2 transcription is not known
Zhang et al., Zhonghua Jie He He Hu Xi Za Zhi 2010
(Ventilator-Induced Lung Injury) :
[ Expression of intercellular cell adhesion molecule-1,
interleukin-10 and the
activation of
activator protein-1 in ventilator induced lung injury in rabbits ]
Byun et al., Biochem Biophys Res Commun 2012
(Inflammation) :
In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a,
interleukin [ IL]-1ß, and IL-6 ) and
activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38,
c-Jun N-terminal kinase (JNK) , and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Walters et al., Mol Immunol 2013
:
Transcription of
interleukin-2 (IL-2) , a pivotal cytokine in the mammalian immune response, is
induced by NFAT and
AP-1 transcriptional activators in stimulated T cells
Paliogianni et al., Transplantation 1995
:
Glucocorticoids ( GC )
inhibit IL-2 gene transcription by interfering with the binding of the nuclear factor
activator protein-1 on the IL-2 promoter
Ivanov et al., J Immunol 1994
:
These experiments also demonstrated a key
role for NF-kappa B and
AP-1 in the transcriptional regulation of the
IL-2 gene by TCR- and Ly6A/E mediated signaling
Rincón et al., EMBO J 1994
:
The transcription factor
AP-1 contributes significantly to the regulation of
interleukin-2 gene transcription during T-cell activation and may play a role in thymocyte development
Pfeuffer et al., J Immunol 1994
:
By contrast, both classes of factors bind simultaneously to the IL-2 promoter, and their tight association with
AP-1 enhances the
IL-2 promoter activity
Petrak et al., J Immunol 1994
:
To explore the
requirements for
AP-1 in
IL-2 production, the AP-1 complex was targeted with a dominant negative mutant c-Jun protein, TAM-67, from which the transactivation domain has been deleted
Tahéri et al., Gastroenterol Clin Biol 1993
(Adenocarcinoma...) :
Northern blot characterization of cellular mRNA revealed that
interleukin 2 enhances the expression of
JUN , FOS and TGF beta which are known to be involved in antiproliferative processes
Su et al., Cell 1994
:
Similar to its effect on IL-2 induction, cyclosporin A ( CsA ) inhibited the synergistic activation of JNK, and a competitive inhibitor of
Jun phosphorylation by JNK
inhibited IL-2 promoter activation
Sung et al., J Biol Chem 1993
:
Stimulation of
interleukin-1 gene transcription may be
caused by the stimulation of transcription factor activities, including those of
AP-1 , by these protein phosphatase inhibitors
Lenczowski et al., Mol Cell Biol 1997
:
While TAM-67 effectively prevented
AP-1 dependent transcription of both the
interleukin-2 and cJun genes, it had no effect on Fas induced cell death, even at limiting levels of Fas signaling
Schwenger et al., Proc Natl Acad Sci U S A 1997
:
c-Jun N-terminal kinase activation
induced by
interleukin 1 or epidermal growth factor was less strongly inhibited by NaSal
Akiyama et al., Nihon Kyobu Shikkan Gakkai Zasshi 1997
(Hypereosinophilic Syndrome...) :
AP-1 is the primary
target for steroid mediated repression of
IL-2 gene transcription, but NF-AT appears to be the main target of cyclosporin
Sansbury et al., Carcinogenesis 1997
(Thymoma) :
Phorbol ester induced morphological changes, ERK activation, calcium dependent
activation of the
c-Jun N-terminal kinase (JNK) ,
interleukin-2 synthesis, and growth inhibition in sensitive but not resistant cells
Hata et al., J Biol Chem 1998
:
Further, FcepsilonRI induced
IL-2 gene activation is
dependent on
c-Jun and a component, SEK1, of its upstream activation pathway
Parra et al., J Immunol 1998
:
The
role of Rel and
activation protein-1 (AP-1) in
IL-2 promoter activity in B7-1- and leukocyte function associated Ag-3 ( LFA. 3 ) -costimulated T cells has been evaluated
O'Neill et al., J Leukoc Biol 1998
:
IRAK-1 has also been implicated in
AP1 induction, Jun amino-terminal kinase (JNK) activation, and
IL-2 induction
Woodside et al., J Immunol 1998
:
However, there has been no direct demonstration that
activator protein-1 is
involved in CD28 dependent costimulation of
IL-2 gene transcription in freshly isolated naive and memory human T lymphocytes ... Scrape loading thus provides an efficient mechanism for intracellular incorporation of macromolecules, and the first direct evidence that c-Fos and
c-Jun are
involved in transcription of the
IL-2 gene within its correct chromosomal context, in resting human T lymphocyte subpopulations
Sundstedt et al., J Immunol 1998
:
The transcription factor
activating protein-1 (AP-1) contributes significantly to the regulation of
IL-2 gene expression during T cell activation and has been suggested to play a unique role in T cell anergy in vitro