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FOSL2 — JUN
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
O/- complex ()
→
Complex of FOSL2-JUN
(directlyIncreases, FOSL2/JUN Activity)
Wang et al., Nat Cell Biol 2007*
Evidence: c-Jun/Fra-2 AP-1 and p50/p65 NF-kappaB complexes synergistically induce RELB promoter activity in ERalpha {Esr1} positive breast cancer cells and c-Jun/Fra-2 induce RELB promoter in ERalpha breast cancer cells
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NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2:
Fra2/JUN complex (FOSL2-JUN)
→
Connexin 43 (GJA1)
(transcription, activates)
Echetebu et al., Mol Hum Reprod 1999*, Mitchell et al., Endocrinology 2005*
Evidence: reporter gene, physical interaction
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NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2:
JUN (JUN)
→
Fra2/JUN complex (FOSL2-JUN)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Kovary et al., Mol Cell Biol 1992*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
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NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2:
JUN (JUN)
→
Fra2 (FOSL2)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Kovary et al., Mol Cell Biol 1992*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
-
NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2:
Fra2/JUN complex (FOSL2-JUN)
→
Fra2 (FOSL2)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Kovary et al., Mol Cell Biol 1992*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
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NCI Pathway Database AP-1 transcription factor network:
JUN (JUN)
→
Fra2/JUN complex (FOSL2-JUN)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUN (JUN)
→
Fra2 (FOSL2)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
Fra2/JUN complex (FOSL2-JUN)
→
Fra2 (FOSL2)
(modification, collaborate)
Murakami et al., Cell Growth Differ 1999*, Bozec et al., Nature 2008*, Suzuki et al., Nucleic Acids Res 1991, Nishina et al., Proc Natl Acad Sci U S A 1990*, Gruda et al., Oncogene 1994*
Evidence: physical interaction
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NCI Pathway Database AP-1 transcription factor network:
JUN/FOS complex (FOS-JUN)
→
Fra2 (FOSL2)
(transcription, activates)
Sonobe et al., Oncogene 1995*, Ng et al., EMBO J 1997*
Evidence: physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Won et al., Mol Pharmacol 2000
:
In AP-1, the basal expression of
Fra-2 and c-Jun proteins and AP-1 DNA binding activity in the adrenal medulla was higher than other tissues tested, but CHX
reduced these protein levels and
AP-1 DNA binding activity
Berry et al., Biochem Pharmacol 2001
:
Supershift assays demonstrated that in control cells,
AP-1 binding activity was
mediated by Jun
D/Fra 2 heterodimers, whereas after vinblastine treatment, AP-1 complexes also containing c-Jun and Fra 1 were present, suggesting that induction of these latter proteins by vinblastine is functionally significant
Erdem et al., J Appl Physiol 2002
(Body Weight) :
We conclude that 1 ) SET elicits a pretranslational stimulatory effect on adrenomedullary CA biosynthetic enzymes, 2 ) another immediate early mRNA product, rather than
FRA-2 , may
contribute to the increase in
AP-1 binding activity in response to SET, and 3 ) SET increases NPY mRNA expression
Wang et al., J Virol 2005
:
IE1 induced
c-Jun phosphorylation, and treatment with SP600125, a selective JNK inhibitor, as well as overexpression of JNK binding domain of JIP1,
blocked IE1 mediated induction of AP-1 and relB promoter activity in NIH 3T3 cells and SMCs. Ectopic expression of c-Jun plus
Fra-2 , but not c-Fos, induced relB promoter activity
Roy et al., Cardiovasc Res 2010
(Disease Models, Animal...) :
Knockdown of Fra-2 significantly blunted O ( 2 ) -induced expression of TGFbeta1 as well as TGFbeta3 in CF. Knockdown of Ask-1 blunted hyperoxia induced Fra-2 gene expression and nuclear localization in CF. Collectively, these observations point towards a central
role of Ask-1 and
Fra-2 in O ( 2 ) -inducible
AP-1 activation and induction of TGFbeta
Suzuki et al., J Virol 1994
(Cell Transformation, Neoplastic) :
We further showed that
Fra-2-c-Jun heterodimer is mainly
responsible for the elevated
AP-1 DNA binding activity in these transformed cells, and we propose that this heterodimer play a crucial role in the transformation induced by these oncogenes
Rutberg et al., Oncogene 1997
:
Exogenous expression of
Fra-2 repressed
AP-1 transcriptional activity in TPA treated keratinocytes, while c-Fos expression activated the AP-1 sequence in calcium treated keratinocytes
Kustikova et al., Mol Cell Biol 1998
(Adenocarcinoma...) :
We found that the enhanced level of
AP-1 in CSML100 cells was
due to high expression of Fra-1 and
Fra-2 proteins, which were undetectable in CSML0 nuclear extracts
Cook et al., Mol Cell Biol 1999
:
c-Fos,
c-Jun , and JunB are
induced rapidly in response to LPA stimulation, whereas Fra-1 and
Fra-2 are induced after a significant lag ... In cells expressing a conditionally active form of Raf-1 ( DeltaRaf-1 : ER ), we observed that selective, sustained activation of Raf-MEK-MAPK was sufficient to induce expression of Fra-1,
Fra-2 , and JunB but, interestingly,
induced little or no c-Fos or
c-Jun