◀ Back to JUN
JUN — JUNB
Pathways - manually collected, often from reviews:
-
NCI Pathway Database AP-1 transcription factor network:
JUNB (JUNB)
→
JUN (JUN)
(modification, collaborate)
Bakiri et al., EMBO J 2000*, Wang et al., J Immunol 2005*, Nakabeppu et al., Cell 1988*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUNB (JUNB)
→
JUN/JUNB complex (JUNB-JUN)
(modification, collaborate)
Bakiri et al., EMBO J 2000*, Wang et al., J Immunol 2005*, Nakabeppu et al., Cell 1988*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUN (JUN)
→
JUN/JUNB complex (JUNB-JUN)
(modification, collaborate)
Bakiri et al., EMBO J 2000*, Wang et al., J Immunol 2005*, Nakabeppu et al., Cell 1988*
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUNB/JUN-FOS complex (JUNB-FOS_JUN)
→
DMTF1 (DMTF1)
(transcription, activates)
Sreeramaneni et al., Mol Cell Biol 2005
Evidence: reporter gene, physical interaction, other species
-
NCI Pathway Database AP-1 transcription factor network:
JUNB (JUNB)
→
JUN-FOS (FOS/JUN)
(modification, collaborate)
Sreeramaneni et al., Mol Cell Biol 2005
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUNB (JUNB)
→
JUNB/JUN-FOS complex (JUNB-FOS_JUN)
(modification, collaborate)
Sreeramaneni et al., Mol Cell Biol 2005
Evidence: physical interaction
-
NCI Pathway Database AP-1 transcription factor network:
JUN-FOS (FOS/JUN)
→
JUNB/JUN-FOS complex (JUNB-FOS_JUN)
(modification, collaborate)
Sreeramaneni et al., Mol Cell Biol 2005
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
Robinson et al., Int J Cancer 2001
(Mouth Neoplasms...) :
Increased expression of
JunB in the transfected cells
resulted in up-regulation of c-Jun and Fra1 and an enhanced
AP-1 activity as demonstrated by transcriptional activation of the prototypic AP-1 dependent promoter, MMP-1 ... Increased expression of
JunB in the transfected cells
resulted in up-regulation of
c-Jun and Fra1 and an enhanced AP-1 activity as demonstrated by transcriptional activation of the prototypic AP-1 dependent promoter, MMP-1
Medicherla et al., Mech Ageing Dev 2001
:
The observed decrease in
AP-1 binding activity in ageing adrenals is most likely
due to decreased expression of the AP-1 activating components ( c-Fos, c-Jun, JunD, etc. ) and increased expression of
JunB , resulting in a switch from transcriptionally active AP-1 complexes observed in young rats to less efficient JunB containing complexes in old rats
Finch et al., J Cancer Res Clin Oncol 2002
(Cell Transformation, Neoplastic...) :
JunB negatively
regulates AP-1 activity and cell proliferation of malignant mouse keratinocytes
Winter et al., Brain Res Mol Brain Res 2002
(Disease Models, Animal...) :
These effects were obviously achieved by cellular modulations directly following axotomy : Whereas
JunB overexpression
attenuated c-Jun induction and simultaneously led to a higher phosphorylation rate of c-Jun in SNC neurons, Bcl-2 overexpression did not influence c-Jun expression, but resulted in a reduced phosphorylation state of c-Jun in transected SNC neurons
Liu et al., Blood 2003
:
Exogenous
JunB restored
AP-1 DNA binding but did not prevent inhibition of macrosialin expression by C/EBPalpha-ER, indicating that JunB is not the only target relevant to inhibition of monopoiesis by C/EBPalpha
Hsu et al., Mol Cell Biol 1992
:
In liver cells, high levels of
c-Fos/c-Jun , c-Fos/JunB, LRF-1/c-Jun, and LRF-1/JunB complexes are present for several hours after the G0/G1 transition, and the relative level of
LRF-1/JunB complexes
increases during G1 ... LRF-1/c-Jun, c-Fos/c-Jun, and c-Fos/JunB activate specific
AP-1 and ATF site containing promoters, and in contrast,
LRF-1/JunB potently
represses c-Fos- and c-Jun mediated activation of these promoters
Friedman et al., Blood Cells Mol Dis 2003
:
In 32DPKCdelta cells, C/EBPalpha-ER strongly inhibits endogenous or exogenous
JunB induction, dependent upon the outer surface of the C/EBPalpha basic region, but does not
inhibit c-Jun , PU.1, or C/EBPbeta expression ... Exogenous
JunB restores
AP-1 DNA binding but does not overcome inhibition of monopoiesis by C/EBPalpha-ER
Kwon et al., Dev Dyn 1992
:
JunB does not
inhibit the induction of
c-Jun during the retinoic acid induced differentiation of F9 cells
Herdegen et al., Neuroscience 1991
(Vagus Nerve Injuries) :
Vagotomy
induced the expression of
c-JUN and JUN D in the nodose ganglion, dorsal motor nucleus of the vagus nerve and nucleus ambiguus, whereas
JUN B was not expressed in these areas, c-JUN and JUN D appeared after 10 h in the nodose ganglion and after 24 h in the dorsal motor nucleus of the vagus nerve with a maximum of immunoreactivity after 48 h
Gurzov et al., Oncogene 2008
(Melanoma...) :
These results indicate that in the absence of
c-Jun ,
JunB can
act as a tumor promoter and inactivation of both, c-Jun and JunB, could provide a valuable strategy for antitumor intervention
Brooks et al., Mol Immunol 1995
(Thymoma) :
Interleukin 1 activation of the
AP-1 transcription complex in murine T cells is
regulated at the level of
Jun B protein accumulation ... Thus, the stimulation of
AP-1 mediated gene expression by IL-1 in EL4 cells is
due to the promotion of
Jun B protein accumulation that, in turn, facilitates Jun B heterodimerization with TPA induced Fra-1 protein, thereby forming an active AP-1 complex
Tanguay et al., Cell Immunol 1994
:
Activation of
AP-1 in primary B lymphocytes by surface immunoglobulin
requires de novo
Jun-B synthesis
Dragunow et al., Brain Res Mol Brain Res 1993
(Brain Ischemia...) :
Activation of central muscarinic receptors with pilocarpine, or block of D2 dopamine receptors with haloperidol, treatments which do not cause neuronal damage, strongly induced Fos and
Jun B in hippocampal and striatal neurons, but only
induced c-Jun very weakly
Hsu et al., Cancer Res 1993
:
Unlike c-Jun,
JunB represses several
AP-1 or activator of transcription factor site containing promoters, and this inhibition is greatly enhanced in the presence of LRF-1
Deng et al., Genes Dev 1993
:
JunB differs from c-Jun in its DNA binding and dimerization domains, and
represses c-Jun by formation of inactive heterodimers
Cook et al., Mol Cell Biol 1999
:
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