ArticleMolecular and cellular biology1995
Casein kinase II phosphorylation site mutations in c-Myb affect DNA binding and transcriptional cooperativity with NF-M.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 85 citations in OpenAlex.
- A phase 2 study of MK-2206 in patients with incurable adenoid cystic carcinoma (Alliance A091104).Cancer · 2024Trial
- Article
- Situational awareness: regulation of the myb transcription factor in differentiation, the cell cycle and oncogenesis.Cancers · 2014Review
- The interaction of MYC with the trithorax protein ASH2L promotes gene transcription by regulating H3K27 modification.Nucleic acids research · 2014Article
- Dynamic subcellular localization of the mono-ADP-ribosyltransferase ARTD10 and interaction with the ubiquitin receptor p62.Cell communication and signaling : CCS · 2012Article
- Casein kinase II phosphorylation regulates alphaNAC subcellular localization and transcriptional coactivating activity.Gene expression · 2005Article
- The human neuroendocrine thyrotropin-releasing hormone receptor promoter is activated by the haematopoietic transcription factor c-Myb.The Biochemical journal · 2003Article
- Protein kinase CK2: structure, regulation and role in cellular decisions of life and death.The Biochemical journal · 2003Review
- Tumorigenic N-terminal deletions of c-Myb modulate DNA binding, transactivation, and cooperativity with C/EBP.Oncogene · 2001Article
- Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage.Molecular and cellular biology · 2001Article
- The highly conserved DNA-binding domains of A-, B- and c-Myb differ with respect to DNA-binding, phosphorylation and redox properties.Nucleic acids research · 2001Article
- The SMRT corepressor is a target of phosphorylation by protein kinase CK2 (casein kinase II).Molecular and cellular biochemistry · 2001Article
- Functional phosphorylation sites in the C-terminal region of the multivalent multifunctional transcriptional factor CTCF.Molecular and cellular biology · 2001Article
- Review
- Hyperphosphorylation and increased proteolytic breakdown of c-Myb induced by the inhibition of Ser/Thr protein phosphatases.Oncogene · 2000Article
- Myeloblastin is a granulocyte colony-stimulating factor-responsive gene conferring factor-independent growth to hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Article
- Article
- Casein kinase II interacts with the bZIP domains of several transcription factors.Nucleic acids research · 1998Article
- Core binding factor cannot synergistically activate the myeloperoxidase proximal enhancer in immature myeloid cells without c-Myb.Molecular and cellular biology · 1997Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphorylation of c-Myb has been implicated in the regulation of the binding of c-Myb to DNA. We show that murine c-Myb is phosphorylated at Ser-11 and -12 in vivo and that these sites can be phosphorylated in vitro by casein kinase II (CKII), analogous to chicken c-Myb. An efficient method to study DNA binding properties of full-length c-Myb and Myb mutants under nondenaturing conditions was developed. It was found that a Myb mutant in which Ser-11 and -12 were replaced with Ala (Myb Ala-11/12), wild-type c-Myb, and Myb Asp-11/12 bound to the A site of the mim-1 promoter with decreasing affinities. In agreement with this finding, Myb Ala-11/12 transactivated better than wild-type c-Myb and Myb Asp-11/12 on the mim-1 promoter or a synthetic Myb-responsive promoter. Similar observations were made for the myeloid-specific neutrophil elastase promoter. The presence of NF-M or an NF-M-like activity abolished partially the differences seen with the Ser-11/12 mutants, suggesting that the reduced DNA binding due to negative charge at positions 11 and 12 can be compensated for by NF-M. Since no direct interaction of c-Myb and NF-M was observed, we propose that the cooperativity is mediated by a third factor. Our data offer two possibilities for how casein kinase II phosphorylation can influence c-Myb function: first, by reducing c-Myb DNA binding and thereby influencing transactivation, and second, by enhancing the apparent cooperativity between c-Myb and NF-M or an NF-M-like activity.
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