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A Mouse Erythroleukemia Cell Line Possessing Friend Spleen Focus‐forming Virus gp55 Transgene and Temperature‐sensitive Mutant p53 Gene

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TLDR
This non‐virus‐producing, mouse erythroleukemia cell line will be useful for the study of mutated p53 function during the induction of erystrodifferentiation or apoptotic change.
Abstract
Two different erythroleukemia cell lines have been established from the splenic lesions of transgenic mice possessing the Friend spleen focus-forming virus (F-SFFV) gp55 gene. One showed a neardiploid karyotype and a temperature-sensitive (ts) p53 mutation, and the other, a hyper-triploid karyotype with double p53 mutations found by single-strand conformation polymorphism (SSCP) analysis. The cell lines both retained No.11 chromosomes on which p53 genes are localized. Another p53 allele in the cell line with the ts-p53 mutation appeared intact in the SSCP analysis of the genomic exon 5. The cells with the ts-mutant p53 gene showed no apparent change with temperature shift in their growth or dimethylsulfoxide-induced differentiation, although the wild-type p53 gene on the other allele was not expressing. This ts-p53val-135 gene made p53-deficient fibroblasts anchorageindependent at 37°C but not at 32°C. This non-virus-producing, mouse erythroleukemia cell line will be useful for the study of mutated p53 function during the induction of erythrodifferentiation or apoptotic change.

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Citations
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Cloning and functional analysis of human p51, which structurally and functionally resembles p53

TL;DR: In p53-deficient cells, p51A induced growth-suppression and apoptosis, and up-regulated p21waf-1 through p53 regulatory elements, and expression of p5I mRNA was found in a limited number of tissues, including skeletal muscle, placenta, mammary glands, prostate, trachea, thymus, salivary gland, uterus, heart and lung.
Journal ArticleDOI

p53 family genes: structural comparison, expression and mutation.

TL;DR: The p53-related genes, p51/p63 and p73, have been isolated respectively from cDNA libraries of skeletal muscle and the brain, and their structural features and biological functions have been compared and it is shown that p51 is functionally rather distant from p53.
Journal ArticleDOI

p51A (TAp63γ), a p53 homolog, accumulates in response to DNA damage for cell regulation

TL;DR: P51A induces differentiation under genotoxic circumstances and there may be cellular factors that control p51A protein stability and transactivating ability, which suggest the possibility that p53-accumulated cells underwent apoptosis without exhibiting the feature of erythroid differentiation.
Journal ArticleDOI

p53 gene family p51(p63)-encoded, secondary transactivator p51B(TAp63α) occurs without forming an immunoprecipitable complex with MDM2, but responds to genotoxic stress by accumulation

TL;DR: Without an interaction with MDM2, p51B(TAp63alpha) may be degraded by proteasome under normal cellular circumstances but stabilized under genotoxic stress by a posttranscriptional mechanism which might involve Ser/Thr phosphorylation.
Journal ArticleDOI

Induction of erythroid differentiation by inhibition of Ras/ERK pathway in a friend murine leukemia cell line.

TL;DR: It is suggested that down-regulation of Ras/ERK signaling pathway may be an essential event in EPO-induced erythroid differentiation in this system.
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Journal ArticleDOI

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Journal ArticleDOI

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Journal ArticleDOI

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Journal ArticleDOI

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TL;DR: It is demonstrated that genomic rearrangements are responsible for p53 gene Jnactivation in these cell lines and that they occur in vivo during the natural progression of Friend virus-induced erythroleukaemia.
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