Healthy mice with an altered c-myc gene: role of the 3′ untranslated region revisited

Langa, Francina; Lafon, Isabelle; Vandormael-Pournin, Sandrine; Vidaud, Michel; Babinet, Charles; Morello, Dominique

doi:10.1038/sj.onc.1204482

Cited by 22 publications

(18 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The inserted Myc consisted of an intron-less cDNA clone, the noncoding first exon with the natural P1/P2 promoter, 1.5 kb of genomic 5ʹ flank containing the normal transcription-regulatory region, and a short stretch of 3ʹ untranslated region (UTR) harboring the Myc major polyadenylation site. The UTR 3ʹ of the polyadenylation signal, which has been shown to be dispensable in vivo (54), was not present in the construct. The Myc coding region also contained an artificial histidine tag added in frame at its 3ʹ end.…”

Section: Generation Of Myc Transgenicsmentioning

confidence: 99%

Novel targeted deregulation of c-Myc cooperates with Bcl-XL to cause plasma cell neoplasms in mice

Cheung¹,

Kim²,

Linden³

et al. 2004

J. Clin. Invest.

View full text Add to dashboard Cite

IntroductionPlasma cell neoplasms (PCNs) in humans comprise multiple myeloma (MM), Ig deposition and heavy-chain diseases, and plasmacytoma (PCT), which occurs as solitary PCT of bone and extramedullary PCT. Several mouse models of human PCN have been developed to study mechanisms of neoplastic plasma cell development and design new strategies for tumor treatment and prevention. Established mouse models of human PCN include tumors that arose spontaneously in old C57BL/KaLwRij mice and that resemble human MM (reviewed in ref. 1), peritoneal PCT that can be induced in strain BALB/c by intraperitoneal injections of proinflammatory agents and further accelerated by infection of mice with transforming retroviruses (reviewed in ref.2), and the transplantation of human MM cells into SCID mice that harbor preimplanted human fetal bone as a nesting ground for the tumor cells (3-5). Currently emerging mouse models of human PCN are based on transgenic expression in B cells of IL-6 (6) and NPM-ALK (7) (fusion protein of nucleophosmin and anaplastic lymphoma kinase), or viral transduction of NPM-ALK in bone marrow cells (8). While all of these models afford valuable insights into the biology of human PCN, many important features of human PCN have not been adequately recapitulated in mice. One such feature with profound implications for pathogenesis, treatment, and prevention of human PCN is the collaboration of deregulated Myc (c-Myc) with tumor suppressor genes of the Bcl-2 family.

show abstract

Section: Generation Of Myc Transgenicsmentioning

confidence: 99%

Novel targeted deregulation of c-Myc cooperates with Bcl-XL to cause plasma cell neoplasms in mice

Cheung¹,

Kim²,

Linden³

et al. 2004

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Binding of auxiliary factors to the coding region of c-myc mRNA is required to impose this control. The 3Ј-UTR of MYC may contribute to RNA stability in some situations, but not others (Aghib and Bishop 1991;Langa et al 2001). MYC protein turnover is also regulated, and there are different subcellular pools of MYC in cells (Sears et al 2000;Tworkowski et al 2002).…”

Section: How Much Myc?mentioning

confidence: 99%

Reconstructing MYC: Figure 1.

Levens¹

2003

Genes Dev.

133

118

View full text Add to dashboard Cite

“…Plusieurs translocations entraînant la perte de son ARE sont décrites dans des hémo-pathies malignes humaines (revue dans [21]). De manière surprenante, cependant, la délétion de la région 3'UTR de c-myc (c-myc D3'UTR ), créée expérimentalement par recombinaison homologue, n'augmente pas la stabilité de l'ARN c-myc D3'UTR et aucune tumeur n'est observée chez la souris exprimant l'ARN muté [23]. Ces résultats, en apparence contradictoires, peuvent s'expliquer par la découverte que plusieurs séquences, dont l'activité dépend du contexte cellulaire, contrôlent la stabilité de l'ARN c-myc.…”

Section: Les Transgressionsunclassified