The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Oncogenic activity of the c-Myc protein requires dimerization with Max
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Citations
Cites
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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
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The Myc/Max/Mad Network and the Transcriptional Control of Cell Behavior
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The novel ATM-related protein TRRAP is an essential cofactor for the c-Myc and E2F oncoproteins
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Interaction with WDR5 Promotes Target Gene Recognition and Tumorigenesis by MYC
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“The obligate partner is Max, a homologous bHLHLZ Myc-associated factor [19,20].”
BackgroundMad Proteins Contain a Dominant Transcription Repression Domain
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Omomyc Reveals New Mechanisms To Inhibit the MYC Oncogene
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Max deletion destabilizes MYC protein and abrogates Eµ- Myc lymphomagenesis
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Metadata
- Authors
- Amati, B., Brooks, M. W., Levy, N., Littlewood, T. D., Evan, G. I., & Land, H.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1993-01
- Volume
- 72
- Issue
- 2
- Pages
- 233-245
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2085213714
- Cited by
- 560
- References
- 5
- FWCI
- 18.58
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.