Gene Plp A
Mostrando 13-24 de 46 artigos, teses e dissertações.
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13. A prolactin family paralog regulates reproductive adaptations to a physiological stressor
Successful species develop strategies to optimize their reproductive performance. This optimization likely includes the evolution of genes that specifically permit reproduction in physiologically challenging conditions. The prolactin (PRL) family gene cluster is one of 25 mouse-specific gene clusters, the majority of which are associated with reproduction. A
National Academy of Sciences.
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14. Genomic Rearrangements Resulting in PLP1 Deletion Occur by Nonhomologous End Joining and Cause Different Dysmyelinating Phenotypes in Males and Females
In the majority of patients with Pelizaeus-Merzbacher disease, duplication of the proteolipid protein gene PLP1 is responsible, whereas deletion of PLP1 is infrequent. Genomic mechanisms for these submicroscopic chromosomal rearrangements remain unknown. We identified three families with PLP1 deletions (including one family described elsewhere) that arose by
The American Society of Human Genetics.
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15. Nodule-Specific Regulation of Phosphatidylinositol Transfer Protein Expression in Lotus japonicus
Phosphatidylinositol transfer proteins (PITPs) modulate signal transduction pathways and membrane-trafficking functions in eukaryotes. Here, we describe the characterization of a gene family from Lotus japonicus that encodes a novel class of plant PITP-like proteins (LjPLPs) and that is regulated in an unusual nodule-specific manner. Members of this gene fam
American Society of Plant Physiologists.
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16. Disease-associated mutations cause premature oligomerization of myelin proteolipid protein in the endoplasmic reticulum
Pelizaeus–Merzbacher disease (PMD) is a dysmyelinating disease caused by mutations, deletions, or duplications of the proteolipid protein (PLP) gene. Mutant forms of PLP are retained in the endoplasmic reticulum (ER), and the resulting accumulation of mutant protein is thought to be a direct cause of oligodendrocyte cell death, which is the primary clinica
National Academy of Sciences.
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17. Jimpy mutant mouse: a 74-base deletion in the mRNA for myelin proteolipid protein and evidence for a primary defect in RNA splicing.
The mouse mutant jimpy carries an X chromosome-linked recessive gene defect that affects the formation of myelin in the central nervous system. To understand the molecular basis of the jimpy mutation, we have examined the expression of mRNAs encoding myelin proteolipid protein (PLP). PLP mRNAs were detectable in jimpy brain RNA at 21 days after birth but wer
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18. Genetic and Immunologic Analyses of PlpE, a Lipoprotein Important in Complement-Mediated Killing of Pasteurella haemolytica Serotype 1
Pasteurella haemolytica serotype 1 is the bacterium most commonly associated with bovine shipping fever. The presence of antibodies against P. haemolytica outer membrane proteins (OMPs) correlates statistically with resistance to experimental P. haemolytica challenge in cattle. Until now, specific P. haemolytica OMPs which elicit antibodies that function in
American Society for Microbiology.
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19. Pelizaeus-Merzbacher disease: a valine to phenylalanine point mutation in a putative extracellular loop of myelin proteolipid.
In the central nervous system, myelin proteolipid protein isoforms (PLP and DM20) play an essential structural role in myelination. It has been shown in several species that myelination is impaired by molecular defects resulting from single base mutations in the PLP gene. We have used DNA amplification by polymerase chain reaction to study the PLP gene codin
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20. Disruption of the compacted myelin sheath of axons of the central nervous system in proteolipid protein-deficient mice.
The isoproteins proteolipid protein (PLP) and DM20, the two major integral membrane proteins of central nervous system (CNS) myelin, are encoded by a single gene on the X chromosome and show a different developmental expression pattern. To investigate their functions in myelin structure and myelination, we produced transgenic mice carrying a targeted alterat
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21. Three contiguous lipoprotein genes in Pasteurella haemolytica A1 which are homologous to a lipoprotein gene in Haemophilus influenzae type b.
An Escherichia coli clone carrying the recombinant plasmid pPH24 has been found to express highly immunoreactive antigens of Pasteurella haemolytica A1. Two or three antigens of approximately 30 kDa were located to both the inner and outer membranes of the E. coli clone and in P. haemolytica A1. From the insert DNA of 8.2 kbp on pPH24, a fragment of 4.6 kbp
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22. Mutation of the proteolipid protein gene PLP in a human X chromosome-linked myelin disorder.
Myelin is a highly specialized membrane unique to the nervous system that ensheaths axons to permit the rapid saltatory conduction of impulses. The elaboration of a compact myelin sheath is disrupted in a diverse spectrum of human disorders, many of which are of unknown etiology. The X chromosome-linked human disorder Pelizaeus-Merzbacher disease is a clinic
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23. Pelizaeus-Merzbacher disease: tight linkage to proteolipid protein gene exon variant.
Pelizaeus-Merzbacher disease (PMD) is a human X chromosome-linked dysmyelination disorder of the central nervous system for which the genetic defect has not yet been established. The jimpy mutation jp of the mouse is an X chromosome-linked disorder of myelin formation. The mutation is at an intron/exon splice site in the mouse gene for proteolipid protein (P
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24. L-allo-threonine aldolase from Aeromonas jandaei DK-39: gene cloning, nucleotide sequencing, and identification of the pyridoxal 5'-phosphate-binding lysine residue by site-directed mutagenesis.
We have isolated the gene encoding L-allo-threonine aldolase (L-allo-TA) from Aeromonas jandaei DK-39, a pyridoxal 5'-phosphate (PLP)-dependent enzyme that stereospecifically catalyzes the interconversion of L-allo-threonine and glycine. The gene contains an open reading frame consisting of 1,014 nucleotides corresponding to 338 amino acid residues. The prot