Gene interactions and pathways from curated databases and text-mining

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MYC — MYCBP

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

Furusawa et al., Int J Oncol 2000 : We have reported that a novel c-Myc binding protein , AMY-1, stimulated the transcription activity of c-Myc and was translocated from cytoplasm to nuclei in a c-Myc dependent manner
Furusawa et al., J Biol Chem 2001 : We have reported that a novel c-Myc binding protein , AMY-1 ( associate of Myc-1 ), stimulated the transcription activity of c-Myc
Satou et al., J Biol Chem 2001 : We have reported that a novel c-Myc binding protein , MM-1, repressed the E-box dependent transcription activity of c-Myc ( Mori, K., Maeda, Y., Kitaura, H., Taira, T., Iguchi-Ariga, S. M. M., and Ariga, H. ( 1998 ) J. Biol. Chem. 273, 29794-29800 )
Furusawa et al., Genomics 2003 : We have reported that a novel c-Myc binding protein , AMY-1, stimulated the transcription activity of c-Myc and was translocated from the cytoplasm to the nucleus in a c-Myc dependent manner
Kimura et al., Int J Oncol 2007 : We have reported that a novel c-Myc binding protein , MM-1, repressed the E-box dependent transcription activity of c-Myc by recruiting the HDAC1 complex via TIF1beta/KAP1, a transcriptional corepressor
Yoshida et al., Exp Cell Res 2008 : We have reported that a novel c-Myc binding protein , MM-1, repressed the E-box dependent transcription activity of c-Myc through TIF1beta/KAP1, a transcriptional corepressor, and that the c-fms gene was a target gene involved in this pathway
Xiong et al., Oncogene 2010 (Neoplasms) : Microarray screening and western analyses revealed that miR-22 repressed the c-Myc binding protein MYCBP , a positive regulator of c-Myc
Narita et al., PloS one 2012 : We have reported that a novel c-Myc binding protein , MM-1, repressed E-box dependent transcription and transforming activities of c-Myc and that a mutation of A157R in MM-1, which is often observed in patients with leukemia or lymphoma, abrogated all of the repressive activities of MM-1 toward c-Myc, indicating that MM-1 is a novel tumor suppressor
Taira et al., Genes Cells 1998 : AMY-1 , which mostly localizes in the cytoplasm, translocates into the nucleus in the S phase of the cell cycle upon an increase of c-myc expression, and may thus control the transcriptional activity of C-MYC