Disease relevance of FSD1L

• Kaposi's sarcoma-associated herpesvirus encodes two related proteins, MIR1 and MIR2, that lead to reduction of the cell surface levels of major histocompatibility complex class I and other polypeptides involved in immune recognition [1].
• The complete nucleotide sequence of the plasmid-mediated MIR-1 beta-lactamase gene confirms its relationship to chromosomally located ampC genes of Enterobacter cloacae. blaMIR-1 is not part of a typical gene cassette but does lie near an element that could be involved in its capture on a plasmid [2].
• Resistance could be transferred by conjugation or transformation with plasmid DNA into Escherichia coli and was due to the production of a beta-lactamase with an isoelectric point of 8.4 named MIR-1 [3].

High impact information on FSD1L

• We herein demonstrate that the GDF8 allele of Texel sheep is characterized by a G to A transition in the 3' UTR that creates a target site for mir1 and mir206, microRNAs (miRNAs) that are highly expressed in skeletal muscle [4].
• Black Mexican Sweetcorn callus transformed with mir1, the gene encoding the 33-kDa cysteine protease, expressed the protease and growth of caterpillars reared on the transgenic callus was reduced 60-80% [5].
• MIR1 and MIR2 do not affect the assembly or transport of their target proteins through the secretory pathway; rather, they act to enhance the selective endocytosis of target chains from the cell surface [1].
• Additionally, two polymorphic markers (Mir1 and Mir2) within the prepro-PTH gene on the short arm of chromosome 11 were analyzed using denaturant gradient gel electrophoresis [6].
• Plasmid profiles of the 11 K. pneumoniae clinical isolates were not identical, but each contained a plasmid from 40 to 60 kb that hybridized with the cloned MIR-1 gene [3].

Biological context of FSD1L

• Both transfer-proficient and transfer-deficient MIR-1 plasmids belonged to the N incompatibility group [3].
• The amino acid sequence of six AmpC beta-lactamases (Eclo1FF, Eclo6FF, Eclo9FF, Eclo10FF, Eclo11FF and Eclo15FF) shared 97-99% homology with the chromosomal AmpC beta-lactamase from E. cloacae P99 and 86-87% homology with those of two plasmid-mediated AmpC beta-lactamases, MIR-1 and ACT-1 [7].

Associations of FSD1L with chemical compounds

• Cefoxitin or imipenem did not induce MIR-1 [3].
• In vitro, MIR-1 hydrolyzed cephalothin and cephaloridine much more rapidly than it did penicillin G, ampicillin, or carbenicillin [3].

Analytical, diagnostic and therapeutic context of FSD1L

• PCR and sequence analysis for the detection of acquired AmpC resistance (by the acquisition of ACT-1/MIR-1, CMY-2, or FOX) revealed that 25 strains contained CMY-2, including 7 of the strains found to have wild-type promoters [8].

References