Identification of the Avian Myeloblastosis Virus Genome

Souza, Lawrence M.; Bergmann, D G; Baluda, M A

doi:10.1007/978-3-642-67984-1_78

Cited by 4 publications

(4 citation statements)

References 2 publications

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“…This suggests that the endonucleases from these viruses may be interchangeable with respect to integration. It is consistent with the observation that AMV, which has genetic lesions in the carboxyterminal domain of pol, can be rescued from a nonproducer cell line by infection with RSV B77 td and can integrate in a normal manner (25). A comparison of the nucleotide se-J.…”

Section: U3-oligodeoxynucleotide Probes (X [Gcacggtgctttt-tctctcc] Ysupporting

confidence: 87%

Circles with two tandem long terminal repeats are specifically cleaved by pol gene-associated endonuclease from avian sarcoma and leukosis viruses: nucleotide sequences required for site-specific cleavage

Duyk

Longiaru

Cobrinik

et al. 1985

J Virol

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Section: U3-oligodeoxynucleotide Probes (X [Gcacggtgctttt-tctctcc] Ysupporting

confidence: 87%

Circles with two tandem long terminal repeats are specifically cleaved by pol gene-associated endonuclease from avian sarcoma and leukosis viruses: nucleotide sequences required for site-specific cleavage

Duyk

Longiaru

Cobrinik

et al. 1985

J Virol

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“…20,21 The oncogenic potential of myb was first observed in birds, when it was discovered that a truncated form of the cellular proto-oncogene, called viral-myb (v-myb), was contained within the AMV and E26 leukemia viruses. [22][23][24] v-myb has deletions at its 5Ј and 3Ј ends, which results in a protein missing a small, but apparently inconsequential, portion of its DNA-binding domain and virtually its entire negative regulatory domain. Loss of the negative regulatory domain is thought to contribute to the transforming ability of the protein.…”

Section: Introductionmentioning

confidence: 99%

Neuromedin U: a Myb-regulated autocrine growth factor for human myeloid leukemias

Shetzline

Rallapalli

Dowd

et al. 2004

Blood

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The c-myb proto-oncogene has been implicated in leukemogenesis, but possible mechanisms remain ill defined. To gain further insight to this process, we used transcript profiling in K562 cells expressing a dominant-negative Myb (MERT) protein. A total of 105 potential Myb gene targets were identified. Neuromedin U (NmU), a peptide affecting calcium transport, underwent the greatest expression change (ϳ 5-fold decrease). To verify a linkage between c-myb and NmU, their mRNA levels were quantitated using realtime polymerase chain reaction in primary acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL), as well as normal hematopoietic cells. We found that c-myb was elevated in AML and ALL samples, but NmU expression was increased only in AML cells. Significantly, only AML cells expressed the cognate receptor of NmU, NMU1R, suggesting the presence of a novel autocrine loop. We examined this possibility in detail. Exogenous NmU "rescued" growth suppression in K562-MERT cells and stimulated the growth of primary AML cells. Short interfering RNA "knockdown" of NmU in K562 cells arrested cell growth. Exposing Indo-1-labeled K562 cells to NmU induced an intracellular Ca ؉؉ flux consistent with engagement of the NMU1R. Combined, these results suggest that NmU expression is related to Myb and that the NmU/NMU1R axis constitutes a previously unknown growth-promoting autocrine loop in myeloid leukemia cells. IntroductionThe proto-oncogene c-myb encodes a transcription factor, Myb, that is expressed predominantly in immature hematopoietic cells [1][2][3] where it plays a critical role in definitive hematopoiesis. 4-6 c-Myb transactivates its target genes by binding to a well-defined consensus sequence, [PyAAC(T/G)G], referred to as the Myb responsive element. 7 Of genes known to be induced by Myb, many regulate cell proliferation, differentiation, and survival including c-myc, [8][9][10][11][12] cdc2, 13 c-kit, [14][15][16] 17 mim1, 18 myeloblastin, 19 and bcl2. 20,21 The oncogenic potential of myb was first observed in birds, when it was discovered that a truncated form of the cellular proto-oncogene, called viral-myb (v-myb), was contained within the AMV and E26 leukemia viruses. [22][23][24] v-myb has deletions at its 5Ј and 3Ј ends, which results in a protein missing a small, but apparently inconsequential, portion of its DNA-binding domain and virtually its entire negative regulatory domain. Loss of the negative regulatory domain is thought to contribute to the transforming ability of the protein. 25 These deletions may have arisen as a result of retroviral insertional mutagenesis because the myb locus is known to undergo retroviral insertion. 22 Further, retroviral insertion of c-myb in chicken and mouse models produces a truncated form of the c-myb gene, which causes B-and T-cell lymphomas [26][27][28][29] and myeloid leukemias, 10,30-32 respectively.In humans, aberrant expression of c-myb has been associated with leukemia 33 as well as a number of solid tumor cancers such as colon cancer. 34 Exposing human c...

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“…v-myb is the transforming oncogene of avian myeloblastosis virus and E26 leukemia virus, both of which cause hematopoietic malignancies in chickens (3,4,24,25,36,42). A conserved cellular protooncogene sequence, c-myb, is present in the genomes of all metazoan species thus far examined (2,11,18).…”

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confidence: 99%

Constitutive expression of a c-myb cDNA blocks Friend murine erythroleukemia cell differentiation.

et al. 1988

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A full-length human c-myb cDNA clone has been isolated from a CCRF-CEM leukemia cell cDNA library. The plasmid vector contains simian virus 40-derived promotor, splice, and polyadenylation sequences as well as a transcription unit for a dihydrofolate reductase cDNA. We have introduced this construct into Friend erythroleukemia (F-MEL) cells and have isolated a number of clones which contain intact and transcriptionally active human c-myb sequences. F-MEL clones expressing the highest levels of the human c-myb mRNA differentiate poorly in response to dimethyl sulfoxide. Two clones which initially expressed low levels of human c-myb transcripts and which differentiated normally were subsequently inhibited in their ability to differentiate when grown in successively higher concentrations of methotrexate, due to amplification and enhanced expression of plasmid sequences. The inhibitory effect on F-MEL differentiation appeared to be independent of the early decline in c-myc transcripts which were normally regulated in all cases examined. Our results indicate that constitutive expression of a nontruncated human c-myb cDNA can exert profound effects on erythroid differentiation and argue for a causal role of c-myb in the F-MEL differentiation process.

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Identification of the Avian Myeloblastosis Virus Genome

Cited by 4 publications

References 2 publications

Circles with two tandem long terminal repeats are specifically cleaved by pol gene-associated endonuclease from avian sarcoma and leukosis viruses: nucleotide sequences required for site-specific cleavage

Circles with two tandem long terminal repeats are specifically cleaved by pol gene-associated endonuclease from avian sarcoma and leukosis viruses: nucleotide sequences required for site-specific cleavage

Neuromedin U: a Myb-regulated autocrine growth factor for human myeloid leukemias

Constitutive expression of a c-myb cDNA blocks Friend murine erythroleukemia cell differentiation.

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