B-MYB is a ubiquitous transcription factor with an essential role in mouse development. Because cells with a disrupted B-MYB gene cannot be obtained, it is still unknown what is the critical function(s) exerted by B-MYB in mammalian cells. In this study we have observed that reducing B-MYB expression in primary human fibroblasts by using RNA interference results in a partial block of the cells in the G2 phase of the cell cycle and cell death. Surprisingly, suppressing B-MYB transcriptional activity with a dominant-negative molecule is without effect, suggesting that its transactivating function is not essential. Only human or murine fibroblasts exposed to high temperature are sensitized to cell death in the presence of dominant-negative B-MYB. This correlates with temperature-dependent binding of endogenous B-MYB to transcriptional regulatory elements of the stress-related gene ApoJ/clusterin. We find that regulation of ApoJ/clusterin by B-MYB is a pro-survival response to thermal stress. Thus, B-MYB is regulated by temperature to activate genes required for cell survival. B-MYB is a ubiquitous transcription factor with an essential role in mouse development. Because cells with a disrupted B-MYB gene cannot be obtained, it is still unknown what is the critical function(s) exerted by B-MYB in mammalian cells. In this study we have observed that reducing B-MYB expression in primary human fibroblasts by using RNA interference results in a partial block of the cells in the G2 phase of the cell cycle and cell death. Surprisingly, suppressing B-MYB transcriptional activity with a dominant-negative molecule is without effect, suggesting that its transactivating function is not essential. Only human or murine fibroblasts exposed to high temperature are sensitized to cell death in the presence of dominant-negative B-MYB. This correlates with temperature-dependent binding of endogenous B-MYB to transcriptional regulatory elements of the stress-related gene ApoJ/clusterin. We find that regulation of ApoJ/clusterin by B-MYB is a pro-survival response to thermal stress. Thus, B-MYB is regulated by temperature to activate genes required for cell survival. B-MYB is a transcription factor that has been implicated in regulation of cell growth, differentiation, and transformation (1Joaquin M. Watson R.J. Cell. Mol. Life Sci. 2003; 60: 2389-2401Crossref PubMed Scopus (92) Google Scholar). It is homologous to the prototype member of the MYB family, the protooncogene c-MYB, which is prevalently expressed in hematopoietic cells where it controls their differentiation and proliferation (2Oh I.H. Reddy E.P. Oncogene. 1999; 18: 3017-3033Crossref PubMed Scopus (420) Google Scholar). All MYB family members bind to the same consensus sequence (C/T)AACNG in in vitro assays, reflecting their high homology in the DNA-binding domain region (2Oh I.H. Reddy E.P. Oncogene. 1999; 18: 3017-3033Crossref PubMed Scopus (420) Google Scholar). It is possible, however, that the different MYB proteins regulate different genes in vivo after post-translational modifications or interaction with specific cofactors (3Ness S.A. Blood Cells Mol Dis. 2003; 31: 192-200Crossref PubMed Scopus (50) Google Scholar, 4Rushton J.J. Davis L.M. Lei W. Mo X. Leutz A. Ness S.A. Oncogene. 2003; 22: 308-313Crossref PubMed Scopus (79) Google Scholar). B-MYB can be considered the most intriguing member of the MYB family because it seems to exert a fundamental function in mammalian development. Firstly, unlike c-MYB and A-MYB, it is expressed ubiquitously. Secondly, B-MYB inactivation in mice causes an early block of development, without formation of the inner cell mass and normal blastocyst (5Tanaka Y. Patestos N.P. Maekawa T. Ishii S. J. Biol. Chem. 1999; 274: 28067-28070Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar). This absolute requirement mirrors the high levels of B-MYB, but not of c-MYB and A-MYB, mRNA observed in mouse embryonal stem cells (5Tanaka Y. Patestos N.P. Maekawa T. Ishii S. J. Biol. Chem. 1999; 274: 28067-28070Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar). B-MYB expression is detected in virtually all mammalian cancer cell lines, and its locus at 20q13 is often amplified or overexpressed in a wide variety of human neoplasias (6Tanner M.M. Grenman S. Koul A. Johannsson O. Meltzer P. Pejovic T. Borg A. Isola J.J. Clin. Cancer Res. 2000; 6: 1833-1839PubMed Google Scholar, 7Bar-Shira A. Pinthus J.H. Rozovsky U. Goldstein M. Sellers W.R. Yaron Y. Eshhar Z. Orr-Urtreger A. Cancer Res. 2002; 62: 6803-6807PubMed Google Scholar, 8Skotheim R.I. Monni O. Mousses S. Fossa S.D. Kallioniemi O.P. Lothe R.A. Kallioniemi A. Cancer Res. 2002; 62: 2359-2364PubMed Google Scholar, 9Albrecht B. Hausmann M. Zitzelsberger H. Stein H. Siewert J.R. Hopt U. Langer R. Hofler H. Werner M. Walch A. J. Pathol. 2004; 203: 780-810Crossref PubMed Scopus (52) Google Scholar). In contrast, the B-MYB gene is not transcribed in differentiated adult mammalian tissues. Although B-MYB mRNA expression is found in highly proliferating human progenitor cells induced to differentiate along the erythroid or granulocytic/monocytic lineage in vitro (10Sala A. Watson R. J. Cell. Physiol. 1999; 179: 245-250Crossref PubMed Scopus (63) Google Scholar), B-MYB protein expression is barely detectable in the spleen and totally absent in the liver, lungs, kidney, adrenal gland, and sympathetic ganglia of adult mice. 1G. Santilli, R. Schwab, R. Watson, C. Ebert, B. J. Aronow, and A. Sala, unpublished data. Initial characterization in cancer cell lines or in immortalized fibroblasts suggested that B-MYB may be required for cell proliferation or survival. B-MYB expression in fibroblasts is growth-regulated and peaks at the G1/S transition phase of the cell cycle (11Lam E.W.F. Robinson C. Watson R.J. Oncogene. 1992; 7: 1885-1890PubMed Google Scholar). Ectopic expression of B-MYB has been shown to increase the number of cells in the S phase (12Sala A. Casella I. Bellon T. Calabretta B. Watson R.J. Peschle C. J. Biol. Chem. 1996; 271: 9363-9367Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar). On the other hand, antisense inhibition of B-MYB results in suppression of clonogenesis (13Sala A. Calabretta B. Proc. Natl. Acad. Sci. U. S. A. 1992; 89: 10415-10419Crossref PubMed Scopus (102) Google Scholar, 14Lin D. Fiscella M. O'Connor P.M. Jackman J. Chen M. Luo L.L. Sala A. Travali S. Apella E. Mercer W.E. Proc. Natl. Acad. Sci. U. S. A.,. 1994; 91: 10079-10083Crossref PubMed Scopus (116) Google Scholar, 15Raschellá G. Negroni A. Sala A. Pucci S. Romeo A. Calabretta B. J. Biol. Chem. 1995; 270: 8540-8545Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar). Whether or not this latter effect is due to a block of cell proliferation or enhanced cell death has not been investigated. Overexpression of B-MYB often promotes cell survival; it has been shown to counteract apoptosis of lymphoid cell lines in culture and to up-regulate the antiapoptotic BCL2 gene (16Grassilli E. Salomoni P. Perrotti D. Franceschi C. Calabretta B. Cancer Res. 1999; 59: 2451-2456PubMed Google Scholar). Ectopic B-MYB expression confers protection to doxorubicin killing in neuroblastoma cells (17Cervellera M. Raschella G. Santilli G. Tanno B. Ventura A. Mancini C. Sevignani C. Calabretta B. Sala A. J. Biol. Chem. 2000; 275: 21055-21060Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar). In monocytic cells, B-MYB suppresses apoptosis and sustains proliferation in the presence of the terminal differentiating cytokine interleukin 6 (18Bies J. Hoffman B. Amanullah A. Giese T. Wolff L.B. Oncogene. 1996; 12: 355-363PubMed Google Scholar). In one recent study, Liu and Greene have observed that MYB proteins are induced by DNA damage to promote neuronal cell death (19Liu D.X. Greene L.A. Neuron. 2001; 32: 425-438Abstract Full Text Full Text PDF PubMed Scopus (118) Google Scholar). However, in our laboratory we have found no evidence of c-MYB, A-MYB, or B-MYB activation in DNA-damaged neuronal cancer cell lines suggesting that more studies are needed to fully understand the role of MYB genes in neuron demise (20Pagnan G. Sala A. Neurosci. Lett. 2003; 336: 163-166Crossref PubMed Scopus (2) Google Scholar). MYB consensus sequences have been found in promoter or enhancer elements of a number of genes. B-MYB can directly or indirectly transactivate ApoJ/clusterin, MYC, B-MYB itself, HIV LTR, collagen, FGF, UCHL1, IGFBP5, BCL2, and a plethora of potential B-MYB, c-MYB, and A-MYB target genes have been identified by microarrays (4Rushton J.J. Davis L.M. Lei W. Mo X. Leutz A. Ness S.A. Oncogene. 2003; 22: 308-313Crossref PubMed Scopus (79) Google Scholar, 16Grassilli E. Salomoni P. Perrotti D. Franceschi C. Calabretta B. Cancer Res. 1999; 59: 2451-2456PubMed Google Scholar, 17Cervellera M. Raschella G. Santilli G. Tanno B. Ventura A. Mancini C. Sevignani C. Calabretta B. Sala A. J. Biol. Chem. 2000; 275: 21055-21060Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar, 21Nakagoshi H. Kanei-Ishii C. Sawazaki T. Mizuguchi G. Ishii S. Oncogene. 1992; 7: 1233-1240PubMed Google Scholar, 22Sala A. De Luca A. Giordano A. Peschle C. J. Biol. Chem. 1996; 271: 28738-28740Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar, 23Sala A. Kundu M. Casella I. Engelhard A. Calabretta B. Grasso L. Paggi M.G. Giordano A. Watson R.J. Khalil K. Peschle C. Proc. Natl. Acad. Sci. U. S. A. 1997; 94: 532-536Crossref PubMed Scopus (91) Google Scholar, 24Marhamati D.J. Sonenshein G.E. J. Biol. Chem. 1996; 271: 3359-3365Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar, 25Johnson L.R. Johnson T.K. Desler M. Luster T.A. Nowling T. Lewis R.E. Rizzino A. J. Biol. Chem. 2002; 277: 4088-4097Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar, 26Tanno B. Negroni A. Vitali R. Pirozzoli M.C. Cesi V. Mancini C. Calabretta B. Raschella G. J. Biol. Chem. 2002; 277: 23172-23180Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 27Long E.M. Long M.A. Tsirigotis M. Gray D.A. Lung Cancer. 2003; 42: 9-21Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar, 28Cicchillitti L. Jimenez S.A. Sala A. Saitta B. Biochem. J. 2004; 378: PubMed Google Scholar). B-MYB cell proliferation and family member is found with B-MYB in vivo and in and proteins (10Sala A. Watson R. J. Cell. Physiol. 1999; 179: 245-250Crossref PubMed Scopus (63) Google Scholar, 22Sala A. De Luca A. Giordano A. Peschle C. J. Biol. Chem. 1996; 271: 28738-28740Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar, M. M. Watson R.J. Oncogene. 2002; PubMed Scopus Google Scholar). B-MYB has been shown to bind to and the M. Watson R.J. J. Biol. Chem. 2003; Full Text Full Text PDF PubMed Scopus Google Scholar). studies a high of of B-MYB and a in which B-MYB cell by gene transcription and the activity of other is B-MYB transcriptional activity is essential or for its in the cell of the B-MYB target genes have been shown to regulate cell and and it is to that at of B-MYB function is its transcriptional However, potential target genes in and binding of B-MYB to regulatory in of mouse cells with a disrupted B-MYB gene has more studies of its in In the study we have different to the role of B-MYB in normal mammalian results its role in the and and cells and in with with the D. Proc. Natl. Acad. Sci. U. S. A. PubMed Scopus Google Scholar). In cells to and with the by the the after and to cells. a of cells, cell RNA mouse cells by by the cells with at Cells with in by of the promoter or its with (17Cervellera M. Raschella G. Santilli G. Tanno B. Ventura A. Mancini C. Sevignani C. Calabretta B. Sala A. J. Biol. Chem. 2000; 275: 21055-21060Abstract Full Text Full Text PDF PubMed Scopus (99) Google with or without or the cells in or at or for and to the after the RNA RNA the to the most B-MYB target sequence is for their to B-MYB protein in to to in and cells. with using a of of for of In we a and proteins in and and a a of in cell by with of and at different with or without in a and for in or in for in cells with a B-MYB expression at for or at temperature with or without with and with of for to by with and in for in We have and a B-MYB that the of human and murine B-MYB. and ApoJ/clusterin In most the same and with different to and to the of RNA or cells using a transcription in a of using of the in and of in a of for ApoJ/clusterin at at and at for by a of at the of the murine promoter with and the to an of the the binding of and of to of the in binding at a at and exposed to an with modifications T. Mol. Cell. Biol. 2001; PubMed Scopus Google Scholar). In fibroblasts in with for at the with cell in of and and for by 6 of at with of protein of or an and to at with at for and in with and in the presence of and DNA in of amplified with ApoJ/clusterin the of B-MYB in and a in the G2 of the that antisense inhibition of B-MYB expression causes suppression of the potential of fibroblasts (13Sala A. Calabretta B. Proc. Natl. Acad. Sci. U. S. A. 1992; 89: 10415-10419Crossref PubMed Scopus (102) Google Scholar). In that study we not the of formation due to a in cell proliferation or survival. RNA interference is to be more antisense and has been to gene We to study the effect of suppressing B-MYB expression with in human embryonal cells are normal human fibroblasts with a B-MYB expression in this cell is with cancer cells or with immortalized murine fibroblasts or cells not cells are for RNA interference to the of B-MYB Cells exposed to a or different of the B-MYB sequences of B-MYB sequence more sequence of B-MYB expression a increase in suggesting that cells may apoptosis the that cells and the not cell death at the of suggesting that a of cells not the cell cycle after G2 and In with this more cells in the phase in the presence of sequence to the of B-MYB with the different response gene or the gene not induced by suggesting that not B-MYB without in but in Cells to have that B-MYB is required for the and of human fibroblasts the cell We that B-MYB regulate the expression of critical target genes. this the its transcriptional activity in a to that with B-MYB DNA-binding domain can a transcriptional dominant-negative molecule to gene expression We have human or murine fibroblasts with a and the B-MYB DNA-binding domain Surprisingly, fibroblasts with the We that fibroblasts to the function of B-MYB transcriptional Although or dominant-negative cells at more to at high with cells to temperature and expression of the dominant-negative protein by that B-MYB transcriptional activity is for proliferation but required for cycle of fibroblasts with or B-MYB dominant-negative in a B-MYB fibroblasts to thermal or cells with the or dominant-negative B-MYB cells exposed to high temperature where and the of cell death by the S.D. the of with cells with the or the dominant-negative B-MYB to with a B-MYB of the B-MYB protein observed in cells B-MYB by and for of the ApoJ/clusterin in B-MYB requirement in cells that it be by thermal stress. We exposed fibroblasts to and observed B-MYB protein by B-MYB protein levels not with temperature in or cells not We however, in that the of B-MYB after of in cells This of the protein ApoJ/clusterin that after of the members c-MYB and A-MYB in fibroblasts transcriptional activity of endogenous B-MYB in different we fibroblasts with the human ApoJ/clusterin to the with or without a in the We have shown that B-MYB can transactivate the ApoJ/clusterin promoter with an In of the causes a of promoter (17Cervellera M. Raschella G. Santilli G. Tanno B. Ventura A. Mancini C. Sevignani C. Calabretta B. Sala A. J. Biol. Chem. 2000; 275: 21055-21060Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar). the ApoJ/clusterin promoter is by high and of the a of promoter activation that B-MYB, and not MYB family is in thermal regulation of the ApoJ/clusterin we have its activity in the presence of the sequence activation of the ApoJ/clusterin promoter is in the presence of B-MYB, but not suggesting that thermal regulation of the ApoJ/clusterin promoter at in the presence of endogenous B-MYB cells with the dominant-negative B-MYB or its Cells and ApoJ/clusterin mRNA levels in cells by or after ApoJ/clusterin mRNA induced by thermal in cells, In contrast, ApoJ/clusterin gene expression totally in the presence of the dominant-negative B-MYB ApoJ/clusterin, but not promoter activity is by dominant-negative B-MYB in cells exposed to of B-MYB causes of ApoJ/clusterin promoter response to thermal cells with the ApoJ/clusterin in its or and exposed to in the the activity the and activity the S.D. cells with the ApoJ/clusterin in the presence of or B-MYB cells exposed to activity in A. cells with the ApoJ/clusterin or a promoter cell factor with or without dominant-negative B-MYB Cells exposed to and activity All in and at B-MYB suppresses transcription of the ApoJ/clusterin fibroblasts with the or of cells by the cells. cells exposed to and at the of the ApoJ/clusterin or for the This with of the B-MYB by have observed that in cells B-MYB protein is after our have shown that B-MYB can be and by the A. De Luca A. Giordano A. Peschle C. J. Biol. Chem. 1996; 271: 28738-28740Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar, S. E. R. Leutz A. J. Mol. 1997; PubMed Scopus Google Scholar, S. P. Watson R.J. Oncogene. 1997; PubMed Scopus Google Scholar, U. O. R. S. Biol. 1997; 7: Full Text Full Text PDF PubMed Scopus Google Scholar). for our that B-MYB be and using different we not find or of B-MYB protein after We B-MYB a temperature-dependent B-MYB that have been shown to be to S. J. B. Res. 2001; PubMed Scopus Google Scholar). induced by causes a in of factor D.J. Liu J. Biol. Chem. 2001; Full Text Full Text PDF PubMed Scopus Google Scholar). B-MYB be by cell at different or reducing or to in B-MYB can the and be detected by the In we have observed that of cell with B-MYB This is due to the formation of a high that is in the and not the of or protein is because not of B-MYB in of cell at B-MYB in a to that of this is not due to of protein because B-MYB is detectable in can a of B-MYB we of after or of B-MYB after and to a by results that the B-MYB is by temperature in a at with a However, other be in this B-MYB to the ApoJ/clusterin in a the mouse ApoJ/clusterin promoter a potential is in a to that of the human that B-MYB can bind to this sequence of the the promoter the suggesting that the interaction is expression of B-MYB can transcription of endogenous ApoJ/clusterin in mouse fibroblasts suggesting that B-MYB regulation of ApoJ/clusterin is We that the to the formation of a protein to bind to target We the of the human or after by of endogenous B-MYB to the ApoJ/clusterin promoter is to in normal and of cells to causes a increase of with the B-MYB, but not and and and This increase is more one that is after of with normal and temperature-dependent binding of B-MYB the human ApoJ/clusterin cells exposed to and for at different cells at normal temperature with cells after cells after cells at normal B-MYB cells after B-MYB cells after B-MYB cells after cells after This with the same ApoJ/clusterin a in which B-MYB may be by temperature to expression of ApoJ/clusterin. of B-MYB regulation that ApoJ/clusterin exert an role in thermal ApoJ/clusterin is by but it is required for the cell to or to is still its role in thermal we exposed ApoJ/clusterin or their to a temperature of for We the cells to normal and we cell by and cells to the suggesting that it of cell death. of DNA by that cell death in cells with a disrupted ApoJ/clusterin gene Thus, of ApoJ/clusterin expression after thermal is a response in mammalian normal or ApoJ/clusterin mice to thermal in a Although the role of B-MYB in mammalian has been is a in our of the regulated by that have been in the not because of the of B-MYB in cell with antisense have not been because it to a cell B-MYB antisense have been with in hematopoietic cells M. M. A. J. 1992; PubMed Google Scholar), but are not in fibroblasts or other cell Sala, unpublished the cells or mice with homologous of the B-MYB gene cannot be (5Tanaka Y. Patestos N.P. Maekawa T. Ishii S. J. Biol. Chem. 1999; 274: 28067-28070Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar). gene be required to the role of B-MYB in However, the recent of has inactivation of gene expression more and In this study, we to the effect of B-MYB in normal human B-MYB function in mammalian we a dominant-negative B-MYB molecule that with its transcriptional dominant-negative D. P. K. 1996; PubMed Scopus Google Scholar), it is not to a transcriptional but not gene B-MYB is detectable in human and its expression is with human cancer cell lines or immortalized murine Thus, we that cells for We different that B-MYB protein expression with different cell death and of cells in the G2 phase of the cell cycle to the B-MYB B-MYB has been shown to increase the G1/S transition of the cell cycle and to be S phase C. Y. R. D. R. Watson R. Oncogene. 1996; 12: Google Scholar). It is that of B-MYB cells to the G2 This is with studies in where it has been shown that which is considered the of mammalian B-MYB, is required for the transition of cells M. H. D.X. T. Ishii S. J. 2002; PubMed Scopus Google Scholar). our results and in is that cell cycle activity by suppression of is by apoptosis in the M. H. D.X. T. Ishii S. J. 2002; PubMed Scopus Google Scholar). Thus, the of DNA observed in cells in the of B-MYB be by apoptosis cell cycle the role of B-MYB in the of we its transcriptional activity our and cells with a high levels of dominant-negative B-MYB. This that of B-MYB target genes is not required in normal Watson and M. M. Watson R.J. Oncogene. 2002; PubMed Scopus Google have shown that B-MYB the block by the family member its transcriptional or cells dominant-negative B-MYB to cells, sensitized to thermal stress. In the of one that of B-MYB target genes is required specific ApoJ/clusterin is a gene by B-MYB (17Cervellera M. Raschella G. Santilli G. Tanno B. Ventura A. Mancini C. Sevignani C. Calabretta B. Sala A. J. Biol. Chem. 2000; 275: 21055-21060Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar). Because thermal ApoJ/clusterin expression in we have B-MYB activity is results that B-MYB the ApoJ/clusterin promoter and that in the of its transcriptional activity thermal regulation is We found that B-MYB to the human ApoJ/clusterin promoter in vivo in a temperature-dependent B-MYB is by but not by DNA damage induced by or not most for this is that B-MYB a which is by the other MYB family the B-MYB DNA-binding domain that are highly to DNA binding cannot B-MYB is S. J. B. Res. 2001; PubMed Scopus Google Scholar). We have observed that at high temperature B-MYB a that is with a to a for the of the ApoJ/clusterin promoter after fibroblasts with a disrupted ApoJ/clusterin gene we that it has a function in thermal our results with in the we can a in which expression of B-MYB is for normal cell cycle of B-MYB regulation at this activity is required for this This a with the where MYB transcriptional activity found to be essential for expression M. H. D.X. T. Ishii S. J. 2002; PubMed Scopus Google Scholar). It is that mammalian B-MYB has to G2 with of the cell cycle this the laboratory W. J.R. J. 2004; PubMed Scopus Google has shown that B-MYB can directly bind to and regulate the expression of genes. It is to that of B-MYB in fibroblasts has no effect in the G1/S transition phase of the cell We and have shown that B-MYB can the activity of the family member and of the which cell D. Fiscella M. O'Connor P.M. Jackman J. Chen M. Luo L.L. Sala A. Travali S. Apella E. Mercer W.E. Proc. Natl. Acad. Sci. U. S. A.,. 1994; 91: 10079-10083Crossref PubMed Scopus (116) Google Scholar, 23Sala A. Kundu M. Casella I. Engelhard A. Calabretta B. Grasso L. Paggi M.G. Giordano A. Watson R.J. Khalil K. Peschle C. Proc. Natl. Acad. Sci. U. S. A. 1997; 94: 532-536Crossref PubMed Scopus (91) Google Scholar, M. M. Watson R.J. Oncogene. 2002; PubMed Scopus Google Scholar). may that B-MYB function not essential in the G1/S the cell the B-MYB transactivating function have to to cell thermal B-MYB is genes to promote cell survival. This is by evidence other that regulation of and by overexpressed B-MYB protein (4Rushton J.J. Davis L.M. Lei W. Mo X. Leutz A. Ness S.A. Oncogene. 2003; 22: 308-313Crossref PubMed Scopus (79) Google Scholar, H. Oncogene. 1997; PubMed Scopus Google In we have the role of B-MYB in mammalian We have shown that B-MYB can be by thermal and the gene ApoJ/clusterin to cell survival. genes are to be by B-MYB. We have observed that B-MYB can bind in a temperature-dependent to the of the its role in thermal is still to be investigated. Santilli, R. Schwab, and A. Sala, in of gene expression in cells to different of damage be to fully understand the role of B-MYB in the at the of and for and the is for the
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