Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-8-12
pubmed:abstractText
The mouse severe combined immune deficiency (scid) phenotype is due to a recessive, autosomal mutation which results in failed development of lymphocytes. An important step during normal lymphocyte development is the germline rearrangement of DNA segments to assemble functional immunoglobulin or T cell receptor genes. scid lymphocytes fail to rearrange these genes properly, resulting in the absence of mature B and T lymphocytes. This mutation was originally mapped to chromosome 16 by linkage to the immunoglobulin lambda light chain genes (Igl-1) and the coat color mutation mahoganoid. We have typed 288 progeny from backcrosses between MOLF/Ei or CAST/Ei and C.B-17-scid for the scid phenotype and nine other loci mapped to the centromeric region of MMU16. We have established a refined map of this region which places the scid gene between Prm-2 and Igl-1. In addition, no recombinations were found between scid and three other loci, VpreB, lambda 5, and D16Mit31, providing markers useful for isolating the scid gene by positional cloning.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0888-7543
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:geneSymbol
&lgr;5, VpreB
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
740-4
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
The mouse severe combined immune deficiency (scid) mutation is closely linked to the B-cell-specific developmental genes VpreB and lambda 5.
pubmed:affiliation
Medical Biology Institute, La Jolla, California 92037.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't