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MYC — RELA

Pathways - manually collected, often from reviews:

• BioCarta cadmium induces dna synthesis and proliferation in macrophages: RELA/p50 complex (RELA) → c-MYC (MYC) (transcription, activates)
• BioCarta mechanism of gene regulation by peroxisome proliferators via ppara: PPAR-alpha/Transcription factors complex (PPARA-JUN_RELA_SP1) → Non-PPRE-Regulated proteins (NOS2A/TNF/MYC/FAT/COX2/NFKBIA) (transcription, inhibits)
  
• FastForward regulation: AHR, RELA → MYC (transcriptional regulation, increase) Kim et al., Oncogene 2000*
  Evidence: REG, PROMACTIVITY, DNABINDING

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: MYC — RELA (physical association, affinity chromatography technology) Chapman et al., Biochem J 2002*
• IRef Biogrid Interaction: MYC — RELA (physical association, affinity chromatography technology) Covic et al., EMBO J 2005*
• IRef Hprd Interaction: RELA — MYC (in vivo) Chapman et al., Biochem J 2002*
• IRef Ophid Interaction: MYC — RELA (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Nakai et al., J Neurochem 2000 : The present results provide additional support for the view that NF-kappaB activation contributes to c-Myc and p53 induction and subsequent apoptosis in an excitotoxic model of Huntington 's disease
Kim et al., Carcinogenesis 2000 (Cell Transformation, Neoplastic...) : Ectopic expression of the transactivating p65 subunit of NF-kappaB in MCF-10F cells induced the c-myc oncogene promoter, which is driven by two NF-kappaB elements, and endogenous c-Myc levels
Soriani et al., Infect Immun 2001 : Myc activation was also associated with an increase of IkappaBalpha turnover, suggesting that elevated Myc expression may be dependent on NF-kappaB
Bhat-Nakshatri et al., Oncogene 2002 (Breast Neoplasms) : Using breast cancer cell lines derived from transgenic mice that overexpress specific oncogene/growth factors in the mammary gland, we show that heregulin but not her2/neu, c-Myc or v-Ha-ras plays a major role in constitutive NF-kappaB activation ... Her2/neu potentiated tumor necrosis factor alpha (TNFalpha)-inducible NF-kappaB activation whereas c-Myc potentiated 12-o-tetracecanyolphorbol-13-acetate ( TPA ) -induced NF-kappaB activation
Chapman et al., Biochem J 2002 (Neoplasms) : Furthermore, NF-kappaB can induce c-Myc gene expression, suggesting that the activities of these factors are functionally linked
Park et al., J Biol Chem 2003 : In light of findings that NF-kappa B stimulates Myc oncoprotein expression in cancers, our findings suggest that NO should be investigated as a prospective therapeutic cancer agent
Matsumura et al., Cell cycle (Georgetown, Tex.) 2003 : c-Myc and E2F1 inhibit NF-kappaB activities induced by TNFalpha or reactive oxygen species
Keller et al., Oncogene 2005 (Burkitt Lymphoma) : Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA binding activity, suggesting that Myc mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells
Yao et al., Oral Dis 2007 (Tongue Neoplasms) : Furthermore, L-685,458 down-regulated cyclin D1, B-cell lymphocytic-leukemia proto-oncogene 2 and c-Myc expressions, which are regulated by the transcription factor NF-kappaB