Motch A and Motch B—Two Mouse Notch Homologues Coexpressed in a Wide Variety of Tissues

Lardelli, Michael; Lendahl, Urban

doi:10.1006/excr.1993.1044

Cited by 128 publications

(58 citation statements)

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“…In Xenopus, expression of a gain-of-function truncated mutant (harboring only the intracellular domain) of X-Notch affects normal development (Coffman et al 1993) and prevents retinal cell differentiation (Dorsky et al 1995). In mammals, three Notch-related genes have been identified: Notchl, Notch2, and Notch3 (Ellisen et al 1991;Weinmaster et al 1991;Del Am• et al 1992;Reaume et al 1992;Weinmaster et al 1992;Lardelli and Lendahl 1993;Kopan and Weintraub 1993;Lardelli et al 1994), and Notchl also appears to control cell-fate determination (Kopan and Weintraub 1993;Kopan et al 1994;Nye et al 1994). Recent studies have shown that Notch signaling pathways have been preserved from Drosophila to mammals and involve binding to the CBF-1/RBP-JK trans-activator (Hsieh and Hayward 1995;Jarriault et al 1995).…”

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confidence: 99%

Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis.

Girard¹,

Hanna²,

Beaulieu³

et al. 1996

Genes Dev.

198

202

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The MMTVD/myc transgenic mice spontaneously develop oligoclonal CD4+CD8 + T-ceU tumors. We used provirus insertional mutagenesis in these mice to identify putative collaborators of c-myc. We found that Notchl was mutated in a high proportion (52%) of these tumors. Proviruses were inserted upstream of the exon coding for the transmembrane domain and in both transcriptional orientations. These mutations led to high expression of truncated Notchl RNAs and proteins (86-110 kD). In addition, many Notchl-rearranged tumors showed elevated levels of full-length Notchl transcripts, whereas nearly all showed increased levels of full-length (330-kD) or close to full-length (280-kD) Notchl proteins. The 5' end of the truncated RNAs were determined for some tumors by use of RT-PCR and 5' RACE techniques. Depending on the orientation of the proviruses, viral LTR or cryptic promoters appeared to be utilized, and coding potential began in most cases in the transmembrane domain. Pulse-chase experiments revealed that the 330-kD Notchl proteins were processed into 110-and 280-kD cleavage products. These results suggest that Notchl can be a frequent collaborator of c-myc for oncogenesis. Furthermore, our data indicate that Notchl alleles mutated by provirus insertion can lead to increased expression of truncated and full-length (330/280-kD) Notchl proteins, both being produced in a cleaved and uncleaved form.

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mentioning

confidence: 99%

Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis.

Girard¹,

Hanna²,

Beaulieu³

et al. 1996

Genes Dev.

198

202

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“…Introduction fication based on published sequences [10][11][12]. The cloned fragment is shown in Fig.…”

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confidence: 99%

“…Three mouse Notch family genes proteins using glutathione-Sepharose 4B beads (Pharmacia)and the in vitro synthesis of [35S]RBP-J~ were done as described previously (mNotchl, mNotch2 and mNotch3) have been identified [4]. The same amount of purified GST-fusion proteins was mixed with [10][11][12]. These three genes encode proteins remarkably similar…”

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confidence: 99%

Functional conservation of mouse Notch receptor family members

et al. 1996

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“…Signaling-Notch1 is a member of a family of proteins (Greenwald and Rubin, 1992); Reaume et al, 1992;Lardelli and Lendahl, 1993;(Lardelli et al, 1994;Lardelli and Lendahl, 1993;Reaume et al, 1992). These molecules are large transmembrane receptors with epidermal growth factor (EGF)-type repeats and Notch family-specific repeats at the extracellular side and tandem ankyrin repeats in the intracellular domain.…”

Section: A Intercellularmentioning

confidence: 99%

“…Notch1 expression is thought to be controlled by extrinsic factors. In the mouse, two other Notch genes have been identified (Lardelli et al, 1994;Lardelli and Lendahl, 1993). Notch2 is also expressed in the anterior presomitic mesoderm.…”

Section: A Intercellularmentioning

confidence: 99%

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

Kappen

Neubüser

Balling

et al. 2007

Birth Defects Research Pt B

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Skeletal variations are common in humans, and potentially are caused by genetic as well as environmental factors. We here review molecular principles in skeletal development to develop a knowledge base of possible alterations that could explain variations in skeletal element number, shape or size. Environmental agents that induce variations, such as teratogens, likely interact with the molecular pathways that regulate skeletal development. Birth Defects Res (Part B), 80:425–450, 2007. © 2007 Wiley‐Liss, Inc.

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Motch A and Motch B—Two Mouse Notch Homologues Coexpressed in a Wide Variety of Tissues

Cited by 128 publications

References 0 publications

Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis.

Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis.

Functional conservation of mouse Notch receptor family members

Molecular basis for skeletal variation: insights from developmental genetic studies in mice

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