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JUN — JUND
Pathways - manually collected, often from reviews:
-
NCI Pathway Database PDGFR-beta signaling pathway:
JUN/JUND complex (JUN-JUND)
→
JUN/JUND complex (JUND-JUN)
(modification, collaborate)
Iavarone et al., J Biol Chem 2003, Boureux et al., J Cell Sci 2005
Evidence: mutant phenotype, assay
-
NCI Pathway Database PDGFR-beta signaling pathway:
JUN/JUND complex (JUN-JUND)
→
JNK family-active (MAPK8/MAPK9/MAPK10)
(modification, collaborate)
Iavarone et al., J Biol Chem 2003, Boureux et al., J Cell Sci 2005
Evidence: mutant phenotype, assay
-
NCI Pathway Database AP-1 transcription factor network:
JUN (JUN)
→
JUN/JUND complex (JUND-JUN)
(modification, collaborate)
Behrens et al., Nat Genet 1999*, Iavarone et al., J Biol Chem 2003, Nicolaides et al., J Biol Chem 1992*, Nakabeppu et al., Cell 1988*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUN (JUN)
→
JUND (JUND)
(modification, collaborate)
Behrens et al., Nat Genet 1999*, Iavarone et al., J Biol Chem 2003, Nicolaides et al., J Biol Chem 1992*, Nakabeppu et al., Cell 1988*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUN/JUND complex (JUND-JUN)
→
JUND (JUND)
(modification, collaborate)
Behrens et al., Nat Genet 1999*, Iavarone et al., J Biol Chem 2003, Nicolaides et al., J Biol Chem 1992*, Nakabeppu et al., Cell 1988*
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
Srivastava et al., J Clin Invest 1999
:
The consequent decrease in the nuclear levels of c-Jun and
JunD leads to diminished binding of
c-Jun/c-Fos and JunD/c-Fos heterodimers to the AP-1 consensus sequence in the TNF promoter and, thus, to decreased transactivation of the TNF gene
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
Gallo et al., Oncogene 2002
:
Furthermore, Menin expression inhibits
Jun N-terminal kinase (JNK) mediated phosphorylation of both
JunD and c-Jun
Yumita et al., Int J Cancer 2003
:
The translation product of the MEN1 gene, menin, has been reported to suppress
JunD mediated
activator protein-1 (AP-1) transactivation and inhibit Ras mediated tumor formation, but its molecular mechanisms and physiologic significance have been poorly elucidated
Yang et al., Pigment Cell Res 2004
(Melanoma) :
There are progressive variations in AP-1 composition in different melanoma cell lines compared with normal melanocytes, in which c-Jun,
JunD and FosB were
involved in
AP-1 complexes ... In w3211, c-Jun,
JunD and Fra-1 were
involved in
AP-1 binding, while in w1205, overall AP-1 binding activity was decreased significantly and supershift binding was detected only with JunD antibodies ... In metastatic c81-46A and A375 cells, only
JunD was
involved in
AP-1 binding activity, but in a third ( c83-2c ) c-Jun, JunD and Fra-1 were present
Ikeo et al., Endocr J 2004
(Multiple Endocrine Neoplasia Type 1) :
JunD-menin interaction
regulates c-Jun mediated
AP-1 transactivation
Zbytek et al., J Cell Physiol 2005
:
CRH also
increased activator protein-1 DNA binding activity with
JunD identified as the most important element
Hilfiker-Kleiner et al., Cardiovasc Res 2006
(Cardiomegaly) :
Over-expression of
JunD in cardiomyocytes
caused enhanced
AP-1 protein-DNA binding, without increasing the transcriptional response from AP-1 or ANP luciferase reporter plasmids at baseline or upon PE stimulation
Smart et al., Hepatology 2006
(Carbon Tetrachloride Poisoning...) :
JunD is a profibrogenic transcription factor
regulated by
Jun N-terminal kinase independent phosphorylation
Huang et al., Nature 2012
:
The menin-JUND interaction blocks
JUN N-terminal kinase (JNK) mediated
JUND phosphorylation and suppresses JUND induced transcription
Tang et al., J Biol Chem 1998
:
Supershift analysis demonstrated that
JunD was the major moiety contributing to AP-1-DNA binding in unstimulated cells and that
c-Jun- , Fra-1-, and Fra-2-DNA binding were
increased whereas JunD-DNA binding was decreased in TGF-beta1 stimulated cells
Shimizu et al., Exp Cell Res 1998
:
The expression of
Jun family members during G1 to S progression was induced biphasically in early and late G1 and the level of
JunD increased markedly at the G1/S, while that of ATF family members was gradually increased along with the G1 to S progression