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|a (TOE)ost10184999
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|a (TOE)10184999
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|a TOE
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|a GDWR
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|a 59
|2 edbsc
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|a E 1.99:anl/cmb/pp--80296
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|a E 1.99:anl/cmb/pp--80296
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|a Rearrangement of RAG-1 recombinase gene in radiation-sensitive ̀̀wasted̀̀ mice
|h [electronic resource]
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|a Washington, D.C. :
|b United States. Dept. of Energy ;
|a Oak Ridge, Tenn. :
|b distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy,
|c 1993.
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|a 21 p. :
|b digital, PDF file.
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|a text
|b txt
|2 rdacontent.
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|a computer
|b c
|2 rdamedia.
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|a online resource
|b cr
|2 rdacarrier.
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|a Published through the Information Bridge: DOE Scientific and Technical Information.
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|a 09/01/1993.
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|a "anl/cmb/pp--80296"
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|a "DE93040883"
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|a Churchill, M.; Weaver, P.; Woloschak, G.E.; Chang-Liu, C.M.; Libertin, C.R.
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|a Topical;
|b 12/31/1993.
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|a Mice recessive for the autosomal gene ̀̀wasted̀̀ (wst) display a disease pattern which includes increased sensitivity to the killing effects of ionizing radiation, immunodeficiency, and neurologic dysfunction. The recent cloning and characterization of recombinase genes (RAG-1/RAG-2) expressed in lymphoid and possibly central nervous system tissues prompted us to examine expression of these genes in DNA repair-deficient/immunodeficient wasted mice. Our results revealed expression of RAG-1 mRNA in spinal cord (but not brain) of control mice; no expression of RAG-1 mRNA was detected in spinal cord or brain from wst/wst mice or their normal littermates (wst/· mice). In thymus tissue, a small RAG-1 transcript (1.0 kb) was detected in wst/wst mice that was not evident in thymus from control mice. In wst/· mice, a two-fold increase in RAG-1 MRNA was evident in thymus tissue. RAG-2 mRNA could only be detected in thymus tissue from wst/· and not from wst/wst or parental control BCF₁ mice. Southern blots revealed a rearrangement/deletion within the RAG-1 gene of affected wasted mice, not evident in known strain-specific parental or littermate controls. These results support the idea that the RAG-1 gene may map at or near the locus for the wasted mutation. In addition, they suggest the importance of recombinase function in normal immune and central nervous system development as well as the potential contribution of this gene family to the normal repair of radiation-induced DNA damage.
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|b W-31109-ENG-38.
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|a Phosphorus 32.
|2 local.
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|a Nerve Cells.
|2 local.
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|a Molecular Biology.
|2 local.
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|a Electrophoresis.
|2 local.
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|a Mice.
|2 local.
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|a Gene Mutations.
|2 local.
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|a Dna Repair.
|2 local.
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|a Dna-cloning.
|2 local.
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|a Gene Recombination Proteins.
|2 local.
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|a Enzyme Induction.
|2 local.
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|a Biological Models.
|2 local.
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|a Spinal Cord.
|2 local.
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|a Basic Biological Sciences.
|2 edbsc.
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|a Argonne National Laboratory.
|4 res.
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1 |
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|a United States.
|b Department of Energy.
|4 spn.
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|a United States.
|b Department of Energy.
|b Office of Scientific and Technical Information.
|4 dst.
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|u http://www.osti.gov/servlets/purl/10184999-QFGoCM/
|z Online Access
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|a .b59568343
|b 03-06-23
|c 05-25-10
|
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|a web
|b 05-25-10
|c f
|d m
|e p
|f eng
|g dcu
|h 0
|i 1
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|a Information bridge
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|s 37b1fd7f-5930-5c1c-b586-90932f94ae22
|
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f |
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|p Can circulate
|a University of Colorado Boulder
|b Online
|c Online
|d Online
|e E 1.99:anl/cmb/pp--80296
|h Superintendent of Documents classification
|i web
|n 1
|