Download Gene Section MYBL2 (v-myb myeloblastosis viral oncogene homolog (avian)-like 2)

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in Oncology and Haematology
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Gene Section
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MYBL2 (v-myb myeloblastosis viral oncogene
homolog (avian)-like 2)
Olesya Chayka, Arturo Sala
Institute of Child Health Molecular Haematology and Cancer Biology Unit 30 Guilford street London,
WC1N 1EH, UK (OC, AS)
Published in Atlas Database: October 2008
Online updated version : http://AtlasGeneticsOncology.org/Genes/MYBL2ID41469ch20q13.html
DOI: 10.4267/2042/44558
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence.
© 2009 Atlas of Genetics and Cytogenetics in Oncology and Haematology
Identity
Protein
Other names: B-MYB, B-Myb, BMYB, MGC15600,
OTTHUMP00000031719
HGNC (Hugo): MYBL2
Location: 20q13.1
Description
704 amino acids, 93kDa protein.
R1, R2, R3 - three repeats 50 amino acids long, R2 and
R3 contain HTH (helix-turn-helix) motives with
unconventional turns required for DNA-binding
activity, R1 serves as a DNA/protein complex
stabilizer; TA contains acidic amino acids and is
responsible for transcriptional activation; RD is
responsible for repression of transactivation function of
B-MYB.
DNA/RNA
Description
49,415 bases DNA with 14 exons.
Transcription
2,731 bases mRNA.
red boxes: untranslated regions; green boxes: coding regions.
Atlas Genet Cytogenet Oncol Haematol. 2009; 13(9)
652
MYBL2 (v-myb myeloblastosis viral oncogene homolog (avian)-like 2)
Chayka O, Sala A
R1, R2 and R3 form DNA-binding domain, TA - transactivation domain, CR - conserved region (the area of homology with c-Myb), RD regulatory domain.
The presence of B-MYB polymorphisms rs2070235
and rs11556379 is associated with a significant
reduction of cancer risk.
Oncogenesis
B-MYB overexpression may result in promotion of
cancer cells survival and proliferation.
Polimorphisms can induce changes in protein
conformation and therefore may in part deactivate BMYB functions.
Expression
Widely expressed, expression is very high in
proliferative cells, embryonic cells, haematopoietic
progenitor cells.
Localisation
Nucleus.
Function
Transcription factor required for cell proliferation, cell
cycle progression, chromosomal stability and
differentiation. B-MYB knockout mice die at E4.5E6.5 due to early developmental arrest.
References
Raschellà G, Negroni A, Sala A, Pucci S, Romeo A, Calabretta
B. Requirement of b-myb function for survival and
differentiative potential of human neuroblastoma cells. J Biol
Chem. 1995 Apr 14;270(15):8540-5
Homology
B-MYB is a member of MYB transcription factors
family, which includes C-MYB and A-MYB, with high
homology within TA and RD regions. DNA-binding
domain is almost identical with that of A-MYB and CMYB and conserved between mouse, human, chicken
and drosophila.
Noben-Trauth K, Copeland NG, Gilbert DJ, Jenkins NA,
Sonoda G, Testa JR, Klempnauer KH. Mybl2 (Bmyb) maps to
mouse chromosome 2 and human chromosome 20q 13.1.
Genomics. 1996 Aug 1;35(3):610-2
Oh IH, Reddy EP. The myb gene family in cell growth,
differentiation and apoptosis. Oncogene. 1999 May
13;18(19):3017-33
Implicated in
Raschellà G, Cesi V, Amendola R, Negroni A, Tanno B,
Altavista P, Tonini GP, De Bernardi B, Calabretta B.
Expression of B-myb in neuroblastoma tumors is a poor
prognostic factor independent from MYCN amplification.
Cancer Res. 1999 Jul 15;59(14):3365-8
Neuroblastoma
Prognosis
Overexpression is thought to be associated with a poor
outcome of the disease.
Oncogenesis
Was reported to be necessary for survival and
differentiation of neuroblastoma cells.
Sala A, Watson R. B-Myb protein in cellular proliferation,
transcription control, and cancer: latest developments. J Cell
Physiol. 1999 Jun;179(3):245-50
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 Oct 1;274(40):28067-70
Hepatocellular carcinoma (HCC)
Oncogenesis
B-MYB is reported to be a probable target of E2F1
transcription
factor,
which
is
dramatically
overexpressed in HCC. There is a clear correlation
between expression level of these two proteins. BMYB overexpression in HCC causes the deregulation
of apoptosis and cell cycle.
Schwab R, Caccamo A, Bettuzzi S, Anderson J, Sala A. BMYB is hypophosphorylated and resistant to degradation in
neuroblastoma: implications for cell survival. Blood Cells Mol
Dis. 2007 Nov-Dec;39(3):263-71
Various cancer
Schwab R, Bussolari R, Corvetta D, Chayka O, Santilli G,
Kwok JM, Ferrari-Amorotti G, Tonini GP, Iacoviello L,
Bertorelle R, Menin C, Hubank M, Calabretta B, Sala A.
Isolation and functional assessment of common, polymorphic
variants of the B-MYB proto-oncogene associated with a
reduced cancer risk. Oncogene. 2008 May 1;27(20):2929-33
Nakajima T, Yasui K, Zen K, Inagaki Y, Fujii H, Minami M,
Tanaka S, Taniwaki M, Itoh Y, Arii S, Inazawa J, Okanoue T.
Activation of B-Myb by E2F1 in hepatocellular carcinoma.
Hepatol Res. 2008 Sep;38(9):886-95
Disease
Amplification of B-MYB was described in breast
carcinomas, liver carcinomas, ovarian carcinomas and
in cutaneous T lymphoma. B-MYB expression was
shown also to be increased in prostate and testicular
malignancies. Moreover, B-MYB expression is notably
increased in metastatic compared to localised prostate
tumours.
Atlas Genet Cytogenet Oncol Haematol. 2009; 13(9)
This article should be referenced as such:
Chayka O, Sala A. MYBL2 (v-myb myeloblastosis viral
oncogene homolog (avian)-like 2). Atlas Genet Cytogenet
Oncol Haematol. 2009; 13(9):652-653.
653