Cloning and characterisation of the abundant cytoplasmic 7S RNA from mouse cells

Balmain, A.; Krumlauf, Robb; Vass, J. Keith; Birnie, G.D.

doi:10.1093/nar/10.14.4259

Cited by 146 publications

(72 citation statements)

References 55 publications

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“…It seems that p50/p50 displays high a nity binding for many distinct kB motifs but provides a strong transcriptional activation only when adopting a speci®c conformation induced by certain kB motifs but not others (Fujita et al, 1992). Interestingly, there are some data that p50/p50 homodimers possessing a high a nity to speci®c kB sites may actually inhibit transcriptional activation of genes by NF-kB factors more potent as transactivators than p50/p50 (reviewed in Baldwin, 1996). Thus, our data on the increase of p50 and p52 expression and the increase of p50-related kB-binding in transformed keratinocytes, suggest that only restricted and speci®c set of kBresponsive genes is under transcription in mouse skin tumors and the transcription of some other kBresponsive genes could be actually inhibited.…”

Section: Discussionmentioning

confidence: 99%

“…The active NF-kB complex is either a homo-or heterodimer composed of proteins from NF-kB/Rel family. Five members of the mammalian NF-kB/Rel family have currently been cloned and characterized; they encode the proteins p50 (NF-kB1), p52 (NF-kB2), p65 (RelA), RelB, and c-Rel (reviewed in Baldwin, 1996;Gilmore et al, 1996). These structurally related interacting proteins bind as dimers to kB motif sequences found in the promoter and enhancer regions of the genes.…”

Section: Introductionmentioning

confidence: 99%

“…These structurally related interacting proteins bind as dimers to kB motif sequences found in the promoter and enhancer regions of the genes. The a nity of speci®c NF-kB factors for di erent DNA kB sites is determined by the di erent combinations of NF-kB/Rel proteins in dimers (reviewed in Matthews and Hay, 1995;Baldwin, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…The primary level of control for NF-kB is mediated through the cytoplasmic inhibitory proteins called IkB (Baldwin, 1996;Whiteside and Israel, 1997). The IkB family include several IkB proteins and proteins p105 and p100 encoded by nf-kb1 and nf-kb2 genes respectively (Gilmore et al, 1996;Whiteside and Israel, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…Previously p100 and p105 were thought to be precursors of NF-kB proteins p52 and p50 (Gilmore et al, 1996;Whiteside and Israel, 1997), however, some recent data indicate that p50 and p105 are generated independently through unique cotranslational processing . When nuclear localization sequences of NF-kB/Rel are covered by IkB, they are retained in the cytoplasm and do not function as active transcription factors (reviewed in Baldwin, 1996;Matthews and Hay, 1995;Siebenlist et al, 1994). Upon stimulation, the IkB proteins are phosphorylated and rapidly degraded through ubiquitin-dependent proteolysis releasing NF-kB to translocate to the nucleus and to activate the expression of target genes (Whiteside and Israel, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Increased expression of p50-NF-κB and constitutive activation of NF-κB transcription factors during mouse skin carcinogenesis

Pérez²,

et al. 1999

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To elucidate the possible role of NF-kB in mouse skin carcinogenesis we studied the expression of p50 (NFkB1), p52 (NF-kB2), p65 (RelA) and IkB-a inhibitor as well as kB-binding activity in adult SENCAR mouse skin, skin papillomas, and squamous cell carcinomas (SCC) generated by a two-stage carcinogenesis protocol. We found that in normal epidermis all of the above proteins were mostly expressed in the cytoplasm of basal cells. Western blot analysis revealed a dramatic increase of p50 and p52 expression in mouse skin tumors starting from the middle stage of promotion. We also found that the level of IkB-a protein in many late papillomas and SCC was lower than in normal epidermis. Results of EMSA showed an increase in kB-binding activity in mouse skin tumors and suggested that p50 is the major component of constitutive kB-binding complexes in normal epidermis and in tumors. It has been shown that nuclear IkB protein Bcl-3 is able to increase p50/p50 homodimer binding to the di erent kB sites in mouse thymocytes. Our ®nding on Bcl-3 overexpression in late papillomas and SCC could explain the selective increase of p50-related kB-binding in mouse skin tumors. Thus, our results strongly suggest the important role of p50 in skin carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Increased expression of p50-NF-κB and constitutive activation of NF-κB transcription factors during mouse skin carcinogenesis

Pérez²,

et al. 1999

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Late-onset neurodegeneration in mice with increased dosage of the proteolipid protein gene

et al. 1998

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Mutations of the proteolipid protein (Plp) gene cause a generalized central nervous system (CNS) myelin deficit in Pelizaeus-Merzbacher disease of man and various tremor syndromes in animal models. X-linked spastic paraplegia is also due to Plp gene mutations but has a different clinical profile and more restricted pathology involving specific tracts and regions. We have shown previously that PLP overexpression in mice homozygous for a Plp transgene results in premature arrest of CNS myelination and premature death. Here, we demonstrate that a low-level increase in Plp gene expression in transgenic mice causes significant axonal degeneration and demyelination with predilection for specific tracts. Following normal motor development, aged mice develop progressive myelin loss, axonal swellings with resultant Wallerian degeneration, and marked vacuolation of the neuropil associated with ataxia, tremor, and seizures. The age of onset and severity of the phenotype is a function of Plp gene dosage. The corticospinal tracts, optic nerve, fasciculus gracilis cerebellum, and brainstem are particularly involved. Although oligodendrocyte cell bodies show little abnormality, their inner adaxonal tongue is often abnormal, suggesting a perturbation of the axon/glial interface that may underlie the axonal changes. We conclude that abnormal expression of an oligodendrocyte-specific gene can cause axonal damage, a finding that is relevant to the pathogenesis of PLP-associated disorders and probably to other myelin-related diseases.

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Co-expression of heparin-binding EGF-like growth factor and related peptides in human gastric carcinoma

et al. 1996

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Heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) is a member of the EGF family of polypeptide growth factors, which includes EGF, transforming growth faaor a (TGF-a), amphiregulin (AR) and betacellulin (BTC). To assess the potential role of HB-EGF in human gastric carcinomas, the expression of HB-EGF and EGF receptor (EGF-R) was examined in normal and cancerous gastric tissues and cultured gastric cancer cell lines. By Northern blot analysis, there was a 4.7-fold increase in HB-EGF mRNA levels in human gastric cancers compared with normal gastric tissues. There was a concomitant 3.9-fold increase in EGF-R mRNA levels in these cancers. lmmunostaining revealed co-localization in 72% of the cancer cells of HB-EGF and EGF-R AR and BTC moieties were not evident by Northern blot analysis. However, using PCR, both AR and BTC mRNA species were demonstrated in normal and cancerous gastric tissues. By Northem blot analysis, HB-EGF, TGF-a. AR, BTC and EGF-R mRNA moieties were co-expressad in KATO 111 and NCLN87 gastric cancer cell lines. Furthermore, HB-EGF, EGF and TGF-a enhanced the growth of both cell lines in a dose-dependent manner. Our findings suggest that HB-EGF is relatively abundant in human gastric cancers and that coexpression of the EGF ligand family may lead to excessive activation of EGF-R in this disorder.o 1996 Wilq-Lks, Inc.Gastric cancer is the 4th most common malignancy in the Western world and a major cause of cancer morbidity and mortality worldwide (Wright et al., 1992). Survival of gastric cancer is determined by the extent of disease and the time of diagnosis. The 5-year survival rate for curative total gastrectomy (% resection) is about 30-40%, whereas the overall 5-year survival rate is less than 20%. A series of changes have been identified as precursors to the intestinal type of gastric cancer, representing apparently sequential steps in the precancerous process. These include superficial gastritis, chronic atrophic gastritis (gland loss), small intestinal metaplasia, colonic metaplasia and dysplasia (Correa, 1992

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Cloning and characterisation of the abundant cytoplasmic 7S RNA from mouse cells

Cited by 146 publications

References 55 publications

Increased expression of p50-NF-κB and constitutive activation of NF-κB transcription factors during mouse skin carcinogenesis

Increased expression of p50-NF-κB and constitutive activation of NF-κB transcription factors during mouse skin carcinogenesis

Late-onset neurodegeneration in mice with increased dosage of the proteolipid protein gene

Co-expression of heparin-binding EGF-like growth factor and related peptides in human gastric carcinoma

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