Historical Background
B-MYB is a member of the Myeloblastosis transcription factor (TF) family which is present in all vertebrates. The other members of the family are A-MYB and c-MYB. c-MYB was the first one to be discovered as a homologue of the v-MYB oncogene carried by two different avian leukemia viruses, Avian Myeloblastosis Virus (AMV) and E26 (Fig. 1) which cause acute myeloblastic leukemia and can also transform immature hematopoietic cells in culture.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsReferences
Baker DJ, Wijshake T, Tchkonia T, LeBrasseur NK, Childs BG, van de Sluis B, et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature. 2011;479(7372):232–6. https://doi.org/10.1038/nature10600.
Chan ASL, Mowla SN, Arora P, Jat PS. Tumour suppressors and cellular senescence. IUBMB Life. 2014;66(12):812–22. https://doi.org/10.1002/iub.1335.
Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains. Exp Cell Res. 1961;25(3):585–621. https://doi.org/10.1016/0014-4827(61)90192-6.
Huang Y, Wu J, Li R, Wang P, Han L, Zhang Z, Tong T. B-MYB delays cell aging by repressing p16 INK4α transcription. Cell Mol Life Sci. 2011;68(5):893–901. https://doi.org/10.1007/s00018-010-0501-9.
Johung K, Goodwin EC, DiMaio D. Human papillomavirus E7 repression in cervical carcinoma cells initiates a transcriptional cascade driven by the retinoblastoma family, resulting in senescence. J Virol. 2007;81(5):2102–16. https://doi.org/10.1128/JVI.02348-06.
Li J, Bai X, Cui S, Fu B, Chen X. Effect of rapamycin on high glucose-induced autophagy impairment, oxidative stress and premature senescence in rat mesangial cells in vitro. Nan Fang Yi Ke Da Xue Xue Bao = J Southern Med University. 2012;32(4):467–71. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22543123.
Litovchick L, Sadasivam S, Florens L, Zhu X, Swanson SK, Velmurugan S, et al. Evolutionarily conserved multisubunit RBL2/p130 and E2F4 protein complex represses human cell cycle-dependent genes in quiescence. Mol Cell. 2007;26(4):539–51. https://doi.org/10.1016/j.molcel.2007.04.015.
Litovchick L, Florens LA, Swanson SK, Washburn MP, Decaprio JA. DYRK1A protein kinase promotes quiescence and senescence through DREAM complex assembly. Genes Dev. 2011;25(8):801–13. https://doi.org/10.1101/gad.2034211.
Masselink H, Vastenhouw N, & Bernards R. (2001). B-myb rescues ras-induced premature senescence, which requires its transactivation domain. Cancer Lett. 171(1), 87–101. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11485831.
Mowla SN, Lam EWF, Jat PS. Cellular senescence and aging: the role of B-MYB. Aging Cell. 2014; https://doi.org/10.1111/acel.12242.
Robinson C, Light Y, Groves R, Mann D, Marias R, Watson R. Cell-cycle regulation of B-Myb protein expression: specific phosphorylation during the S phase of the cell cycle. Oncogene. 1996;12(9):1855–64. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8649845.
Sadasivam S, DeCaprio JA. The DREAM complex: master coordinator of cell cycle-dependent gene expression. Nat Rev Cancer. 2013;13(8):585–95. https://doi.org/10.1038/nrc3556.
Sadasivam S, Duan S, DeCaprio JA. The MuvB complex sequentially recruits B-Myb and FoxM1 to promote mitotic gene expression. Genes Dev. 2012;26(5):474–89. https://doi.org/10.1101/gad.181933.111.
Saville MK & Watson RJ. (1998). The cell-cycle regulated transcription factor B-Myb is phosphorylated by Cyclin A/Cdk2 at sites that enhance its transactivation properties. Oncogene. 1998;17(21):2679–89. https://doi.org/https://dx.doi.org/10.1038/sj.onc.1202503.
Schmit F, Korenjak M, Mannefeld M, Schmitt K, Franke C, von Eyss B, et al. LINC, a human complex that is related to pRB-containing complexes in invertebrates regulates the expression of G2/M genes. Cell Cycle. 2007;6(15):1903–13. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/17671431.
Tanaka Y, Patestos NP, Maekawa T, Ishii S. B-myb is required for inner cell mass formation at an early stage of development. J Biol Chem. 1999;274(Icm):28067–70. https://doi.org/10.1074/jbc.274.40.28067.
Tarasov KV, Tarasova YS, Tam WL, Riordon DR, Elliott ST, Kania G, et al. B-MYB is essential for normal cell cycle progression and chromosomal stability of embryonic stem cells. PLoS One. 2008;3(6):e2478. https://doi.org/10.1371/journal.pone.0002478.
W-FLam E, JWatson R. An E2F-binding site mediates cell-cycle regulated repression of mouse B-myb transcription. EMBO J. 1993;12(7):2705–13.
Ye H, Li L, Guo H, Yin Y. MYBL2 is a substrate of GSK3-like kinase BIN2 and acts as a corepressor of BES1 in brassinosteroid signaling pathway in Arabidopsis. Proc Natl Acad Sci USA. 2012;109(49):20142–7. https://doi.org/10.1073/pnas.1205232109.
Zhan M, Riordon DR, Yan B, Tarasova YS, Bruweleit S, Tarasov KV, et al. The B-MYB transcriptional network guides cell cycle progression and fate decisions to sustain self-renewal and the identity of pluripotent stem cells. PLoS One. 2012; https://doi.org/10.1371/journal.pone.0042350.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2018 Springer International Publishing AG
About this entry
Cite this entry
Kumari, R., Jat, P. (2018). B-Myb. In: Choi, S. (eds) Encyclopedia of Signaling Molecules. Springer, Cham. https://doi.org/10.1007/978-3-319-67199-4_101529
Download citation
DOI: https://doi.org/10.1007/978-3-319-67199-4_101529
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-67198-7
Online ISBN: 978-3-319-67199-4
eBook Packages: Biomedical and Life SciencesReference Module Biomedical and Life Sciences