New light on Myc and Myb. Part I. Myc.

Lüscher, Bernhard; Eisenman, R N

doi:10.1101/gad.4.12a.2025

Cited by 379 publications

(202 citation statements)

References 96 publications

(135 reference statements)

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“…4). One of these, GSK3, phosphorylates Myc within the proline/glutamine-rich domain but little else is known about this interaction at present (Luscher & Eisenman, 1990a). CKII multiply phosphorylates c-Myc in vitro at two distinct regions, corresponding to amino acids 240-262 and 342-357 in the human c-Myc (Fig.…”

Section: Nf-kbmentioning

confidence: 99%

Nuclear protein phosphorylation and growth control

Meek

Street

1992

Biochemical Journal

136

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Section: Nf-kbmentioning

confidence: 99%

Nuclear protein phosphorylation and growth control

Meek

Street

1992

Biochemical Journal

136

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“…c-Myc, a nuclear proto-oncogene product, is a key protein in cell cycle progression, cell transformation and apoptosis (see reviews: Lu Èscher & Eisenman 1990;Packham & Cleveland 1995;Henriksson & Lu Èscher 1996;Hoffman et al 1996;Ryan & Birnie 1996;Prendergast 1999). Structurally, c-Myc is composed of several characteristic domains, including myc boxes located near the N-terminus, an acidic region at the centre, and a basic/helix-loop-helix/leucine zipper (bHLH-Z) near the C-terminus.…”

Section: Introductionmentioning

confidence: 99%

MSSP promotes ras/myc cooperative cell transforming activity by binding to c‐Myc

Niki¹,

Izumi²,

Saëgusa³

et al. 2000

Genes to Cells

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Background: MSSPs, myc single strand binding proteins, were originally identi®ed as proteins recognizing a putative replication origin/transcriptional enhancer in the human c-Myc gene. The cDNAs encoding four of the family proteins, MSSP-1, MSSP-2, Scr2 and Scr3, were cloned. These proteins carry two copies of the putative RNA binding domains, RNP-A and RNP-B, and have been suggested to participate in DNA replication and cell cycle progression from the G 1 to the S phase.

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“…Activation of c-myc is found in a variety of human tumors, its deregulation often being one component of multistage carcinogenesis. 3,4 Aberrant expression of c-myc has been implicated in a wide variety of experimentally induced tumors. 5 The precise mechanism(s) by which myc activation contributes to oncogenesis is not completely defined.…”

Section: Introductionmentioning

confidence: 99%

“…Myc is a DNA-binding phosphoprotein which can function as a transcriptional activator. 3,6 Expression of c-myc is an important signal both for entry into, and continued passage through, the cell cycle. 7,8 It has also been shown that cmyc expression can induce apoptosis.…”

Section: Introductionmentioning

confidence: 99%

V-myc in a simple, single gene retroviral vector causes rapid induction of leukemia and concomitant apoptosis following bone marrow transplantation

Dolnikov

Millington

et al. 1998

Leukemia

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We have previously developed an in vivo model of leukemogenesis utilizing mice reconstituted with genetically modified bone marrow cells. Based on those studies, a new single gene retroviral vector has been engineered which efficiently transfers vmyc into immature murine bone marrow cells. All reconstituted mice developed leukemia with a short latency period (5-11 weeks). In addition to hyperproliferation associated with elevated levels of PCNA, extensive apoptosis was also observed in all leukemic animals with p53 accumulating in the apoptotic cells. Whereas bax encoded protein, an effector of p53 apoptotic activity was detected in apoptotic cells, p21 Waf1 protein, a potential mediator of p53 growth suppression was not detected in these cells suggesting that v-myc-induced apoptosis was independent of the ability of p53 to induce p21 Waf1 . These results indicate that apoptosis, a part of the cellular response to v-myc expression, does not prevent leukemia development and that hyperproliferation rather than abrogation of oncogeneinduced apoptosis appears to be a critical event in v-mycinduced leukemia.

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New light on Myc and Myb. Part I. Myc.

Cited by 379 publications

References 96 publications

Nuclear protein phosphorylation and growth control

Nuclear protein phosphorylation and growth control

MSSP promotes ras/myc cooperative cell transforming activity by binding to c‐Myc

V-myc in a simple, single gene retroviral vector causes rapid induction of leukemia and concomitant apoptosis following bone marrow transplantation

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