TheIL-1? and ? genes are closely linked (&lt;70 kb) on mouse chromosome 2

Silver, Andrew; Masson, W.K.; George, Andrew M.; Adam, Julie; Cox, Roger

doi:10.1007/bf01233095

Cited by 24 publications

(14 citation statements)

References 29 publications

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“…However, pulsed field gel electrophoretic analyses of six AMLs has provided no evidence of structural rearrangement in an 800 kb F region sequence encoding both IL-la and p genes (Silver et al, 1990(Silver et al, , 1991. This, together with the evidence presented here on the site-specific breakage of chromosome 2, tends now to favour an AML-initiating mechanism involving loss of a critical gene or genes from chromosome 2 of target cells (Blatt and Sachs, 1988;Ponder, 1988).…”

Section: Discussionmentioning

confidence: 63%

Murine Radiation Myeloid Leukaemogenesis: A Possible Role for Radiation‐Sensitive Sites on Chromosome 2

Breckon

Papworth

Cox

1991

Genes Chromosomes & Cancer

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There is a paucity of informative data on the potentially important role of specific sites of chromosomal instability in oncogenic processes. Chromosome 2 deletions and rearrangements are known to characterise radiation-induced acute myeloid leukaemia in the mouse. Here we statistically establish a concordance between chromosome 2 breakpoint clusters in these leukaemias and chromosome 2 rearrangements carried at a high in vivo frequency by progeny of irradiated haemopoietic cells. Mechanisms of radiation myeloid leukaemogenesis are discussed with respect to multiple radiation-sensitive sites encoded on chromosome 2 and the possible influence of genomic imprinting on inductive processes.

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Section: Discussionmentioning

confidence: 63%

Murine Radiation Myeloid Leukaemogenesis: A Possible Role for Radiation‐Sensitive Sites on Chromosome 2

Breckon

Papworth

Cox

1991

Genes Chromosomes & Cancer

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“…IL-1 consists of two molecular species, IL-1a and b, which are derived from two distinct genes located 50 kb apart on chromosome 2 of the mouse genome (D'Eutachio et al, 1987;Silver et al, 1990). IL-1, especially IL-1b has diverse actions in the brain and there is considerable evidence implicating it in neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

Suppression of oxidative neuronal damage after transient middle cerebral artery occlusion in mice lacking interleukin-1

Ohtaki¹

2003

Neuroscience Research

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Interleukin-1 (IL-1) contributes to ischemic neurodegeneration. However, the mechanisms regulating action of IL-1 are still poorly understood. In order to clear this central issue, mice that were gene deficient in IL-1a and b (IL-1 KO) and wild-type mice were subjected to 1-h transient middle cerebral artery occlusion (tMCAO). Expression levels of IL-1b and IL-1 receptor I (IL-1RI) were then examined. Generation of peroxynitrite and the expression of mRNAs for nitric oxide synthase (NOS) subtypes were also determined. Immunostaining for IL-1b was increased from 6 h and peaked at 24 h after tMCAO in the microglia and macrophage. The immunoreactivities of IL-1RI were increased progressively in the microvasculature and neuron-like cells of the ipsilateral hemisphere. Infarct volumes were significantly lower in IL-1 KO mice compared with wild-type mice 48 h after tMCAO (P B/0.01). The immunoreactivities of 3-nitro-L-tyrosine were determined in the neurons and microvasculature 24 h after tMCAO and were significantly decreased in the IL-1 KO mice compared to wild-type mice. In addition, expression levels of NOS mRNA in IL-1 KO mice were lower than that measured in wild-type mice. These results indicate that IL-1 is up-regulated and may play a role in neurodegeneration by peroxynitrite production during ischemia. #

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“…T he potent proinflammatory cytokine interleukin-1 (IL-1) is synthesized in two isoforms (designated IL-la and IL-1[3) encoded by distinct, chromosomally linked genes (1)(2)(3). Both forms of IL-1 are synthesized as 31-kD intracellular precursors that are cleaved to the 17-kD mature cytokines found in culture supernatants and extracellular fluids (4).…”

mentioning

confidence: 99%

Mice deficient in IL-1beta manifest impaired contact hypersensitivity to trinitrochlorobenzone.

Shornick

Togni

Mariathasan

et al. 1996

The Journal of Experimental Medicine

228

133

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SummaryMice rendered deficient in IL-1[3 by gene targeting in embryonic stem cells develop and grow normally in a protected laboratory environment. Endotoxin-stimulated peritoneal macrophages from IL-l~-deficient mice showed normal synthesis and cellular release of IL-lct after treatment with 5 mM ATP demonstrating that IL-113 is not necessary for expression and release of the IL-lot isoform. Mice deficient in IL-I~ showed unaltered sensitivity to endotoxic shock, with or without pretreatment with D-galactosamine. In contrast, IL-lJ3-deficient mice showed defective contact hypersensitivity responses to topically applied trinitrochlorobenzene (TNCB). This defect could be overcome either by application of very high doses of sensitizing antigen, or by local intradermal injection of recombinant IL-1[3 immediately before antigen application. These data demonstrate an essential role for IL-1[3 in contact hypersensitivity and suggest that IL-1{3 acts early during the sensitization phase of the response. They suggest an important role for 1I.-1(3 in initiation of the host response at the epidermal barrier.

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TheIL-1? and ? genes are closely linked (<70 kb) on mouse chromosome 2

Cited by 24 publications

References 29 publications

Murine Radiation Myeloid Leukaemogenesis: A Possible Role for Radiation‐Sensitive Sites on Chromosome 2

Murine Radiation Myeloid Leukaemogenesis: A Possible Role for Radiation‐Sensitive Sites on Chromosome 2

Suppression of oxidative neuronal damage after transient middle cerebral artery occlusion in mice lacking interleukin-1

Mice deficient in IL-1beta manifest impaired contact hypersensitivity to trinitrochlorobenzone.

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