Gene interactions and pathways from curated databases and text-mining

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JUN — JUNB

Pathways - manually collected, often from reviews:

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