Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six R sequences have been described as members of a new family of dispersed repetitive DNA in the mouse genome (Gebhard et al., 1982). Several sequenced regions were extended in the 5' direction (R1, R2 and R6) and two new sequences were determined (R7 and R8). On the basis of our sequence and blot hybridization data it is concluded that the R sequence are adjacent to the so-called small Bam family (Fanning, 1982), which in turn runs into the MIF sequence part (Brown & Piechaczyk, 1983) of the large Bam sequences (Meunier-Rotival et al., 1982). In one of our clones a sequence of 1290 base-pairs comprises MIF, Bam and R sequences in a contiguous arrangement which seems to be characteristic of the long repeat unit of the mouse genome. Several repeat units were found to be truncated within their Bam or R sequence parts. Evidence is also reported for transposition events involving R sequences; for instance of one R sequence (R1) into another (R7). Two R sequences (R1 and R4) have apparently been transposed together with part of the adjacent Bam sequences. Truncation and transposition events may also explain the imbalance of copy numbers within the large repeat unit (25,000 to 50,000 for the small Bam sequences and 100,000 for the R sequences). The spreading of R sequences and other interspersed DNA sequences within the mouse genome may have occurred by transposition events on the DNA level and/or by transcription, retrotranscription and insertion processes.
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PMID:Organization of the R family and other interspersed repetitive DNA sequences in the mouse genome. 631 40

Successful lung transplantation has been limited by the high incidence of acute graft rejection. There is mounting evidence that the stress response gene heme oxygenase-1 (HO-1) and/or its catalytic by-product carbon monoxide (CO) confers cytoprotection against tissue and cellular injury. This led us to hypothesize that CO may protect against lung transplant rejection via its anti-inflammatory and antiapoptotic effects. Orthotopic left lung transplantation was performed in Lewis rat recipients from Brown-Norway rat donors. HO-1 mRNA and protein expression were markedly induced in transplanted rat lungs compared to sham-operated control lungs. Transplanted lungs developed severe intraalveolar hemorrhage, marked infiltration of inflammatory cells, and intravascular coagulation. However, in the presence of CO exposure (500 ppm), the gross anatomy and histology of transplanted lungs showed marked preservation. Furthermore, transplanted lungs displayed increased apoptotic cell death compared with the transplanted lungs of CO-exposed recipients, as assessed by TUNEL and caspase-3 immunostaining. CO exposure inhibited the induction of IL-6 mRNA and protein expression in lung and serum, respectively. Gene array analysis revealed that CO also down-regulated other proinflammatory genes, including MIP-1alpha and MIF, and growth factors such as platelet-derived growth factor, which were up-regulated by transplantation. These data suggest that the anti-inflammatory and antiapoptotic properties of CO confer potent cytoprotection in a rat model of lung transplantation.
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PMID:Carbon monoxide induces cytoprotection in rat orthotopic lung transplantation via anti-inflammatory and anti-apoptotic effects. 1281 27