Gene interactions and pathways from curated databases and text-mining

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JUN — JUND

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

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