Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Two proteins,
PS1
and PS2, were detected in the culture medium of Corynebacterium glutamicum and are the major proteins secreted by this bacterium. No enzymatic activity was identified for either of the two proteins. Immunologically cross-reacting proteins were found in a variety of C. glutamicum strains but not in the coryneform Arthrobacter aureus. The gene encoding
PS1
, csp1, was cloned in lambda gt11 using polyclonal antibodies raised against
PS1
to screen for producing clones. The csp1 gene was expressed in Escherichia coli, presumably from its own promoter, and directed the synthesis of two proteins recognized by anti-
PS1
antibodies. The major protein band, of lower M(r), was detected in the periplasmic fraction. It had the same M(r) as the
PS1
protein band detected in the supernatant of C. glutamicum cultures and presumably corresponds to the mature form of
PS1
. The minor protein band appears to be the precursor form of
PS1
. The nucleotide sequence of the csp1 gene was determined and contained an open reading frame encoding a polypeptide with a calculated molecular weight of 70,874, with a putative signal peptide with a molecular weight of 4411. This is consistent with the M(r) determined for
PS1
from C. glutamicum culture supernatant and E. coli whole-cell extracts. The NH2-half of the deduced amino acid is similar (about 33% identical residues and 52% including similar residues) to the secreted antigen 85 protein complex of Mycobacterium. The csp1 gene in C. glutamicum was disrupted without any apparent effect on growth or viability.
Mol
Microbiol 1992 Aug
PMID:Cloning and nucleotide sequence of the csp1 gene encoding PS1, one of the two major secreted proteins of Corynebacterium glutamicum: the deduced N-terminal region of PS1 is similar to the Mycobacterium antigen 85 complex. 140 74
Escherichia coli K-12 strain
PS1
-28-37 carries the multicopy plasmid pPSO28-37 containing a DNA fragment coding for two of the proteins that enable bacteria to utilize sucrose as sole carbon source. One of the different gene products of the plasmid is the outer membrane protein, ScrY. This protein was isolated and purified by chromatography across a gel filtration column. Reconstitution experiments with lipid bilayer membrane demonstrated that ScrY formed ion-permeable channels with properties very similar to those of general diffusion pores of enteric bacteria. The presence of sugars in the aqueous phase led to a dose-dependent block of ion transport through the channel, like the situation found with LamB (maltoporin) of Escherichia coli and Salmonella typhimurium. The binding constants of a variety of different sugars were determined. The stability constant for malto-oligosaccharide binding increased with increasing numbers of glucose residues. Disaccharides generally had a larger binding constant than monosaccharides. The binding of different sugars to ScrY and LamB of E. coli is discussed with respect to the kinetics of sugar movement through the channel.
Mol
Microbiol 1991 Sep
PMID:The sugar-specific outer membrane channel ScrY contains functional characteristics of general diffusion pores and substrate-specific porins. 172 60
The isolated polysaccharide chain,
PS-1
, of the Bordetella pertussis endotoxin was examined by isoelectric focusing, SDS-polyacrylamide gel electrophoresis and gel filtration for heterogeneity and for possible contamination by the parent endotoxin. This polysaccharide, previously found to be a very potent, macrophage-dependent, polyclonal B-cell activator and to mediate the specific binding of the endotoxin to macrophages, stimulated the interleukin 1 (IL 1) secretion by human monocytes; its potency was similar to that measured for the endotoxin. It was concluded that endotoxin-induced IL 1 production may be initiated by the interaction of the polysaccharide chain of the B. pertussis endotoxin and a specific structure present on macrophages.
Mol
Immunol 1984 May
PMID:Interleukin 1 secretion by human monocytes stimulated by the isolated polysaccharide region of the Bordetella pertussis endotoxin. 633 May 37
The fluorescence lifetime and quantum yield as a function of single picosecond laser pulse intensity were experimentally studied in chloroplasts and subchloroplast particles. The intensity of laser pulse were changed from 3 x 10(12) to 10(17) photon/cm2. To explain experimental results it was considered that energy transport in the light harvesting antenna occurs by localised excitons. Parameters governing dynamic of electronic excitation within light harvesting antenna were determined. The diffusion coefficient was found to be 2 x 10(-2) cm2sec-1; diffusion length L greater than or equal to 900 A, energy transfer probability W approximately 10(12)sec-1. The rate of constant of energy transfer from light harvesting antenna to
PS1
and PS2 reaction centers and effectiveness of the exciton capture by the PS2 reaction center were estimated.
Mol
Biol (Mosk)
PMID:[Dynamics of electronic excitation in the photosynthetic pigment apparatus]. 740 8
Three synthetic promoters,
PS1
, PS2 and PS3, which differ in their core promoter elements, were studied in vivo and in vitro. Whereas an increased homology score correlates with higher rates of RNA polymerase binding, it does not correlate with activity in vivo. Permanganate probing in vivo reveals that
PS1
, which exhibits the lowest homology score, is rate-limited during the early phase of promoter-RNA polymerase interactions. By contrast, PS2 and PS3, with higher homology scores, are limited at a late step involving an open DNA region spanning from +6 to +12, indicating a stalling of RNA polymerase. These complexes disappear upon treatment of cells with rifampicin and are replaced by open complexes covering the start site. Because initiated complexes are selectively insensitive to rifampicin action, this confirms that RNA polymerase stalled at +6 to +12 has initiated RNA synthesis. Kinetic studies indicate that the enzyme is released slowly from this position and that this slow release appears to be responsible for the low promoter activity. For PS3, which exhibits the highest homology score and which binds RNA polymerase most efficiently, the release of the stalled complex is particularly slow. PS3 is found to be the weakest of the three promoters in vivo. These results support models in which promoter activity can be determined by various rate limiting steps, including those following the formation of open complexes and even the initiation of RNA synthesis.
J
Mol
Biol 1994 Jun 17
PMID:Stalling of Escherichia coli RNA polymerase in the +6 to +12 region in vivo is associated with tight binding to consensus promoter elements. 800 61
Phased A-tract sequences were inserted in the upstream region of three synthetic promoters known to encompass different rate-limiting steps within the pathway of RNA polymerase-promoter interaction (Ellinger et al., accompanying paper). Promoter
PS1
, which is rate-limited in complex formation, was stimulated by A-tracts in vivo. Permanganate probing showed that the stimulation is due to an enhanced ability to compete for limiting RNA polymerase in vivo, leading to the increased formation of open complexes. By contrast, promoters PS2 and PS3, which are rate-limited in steps following open complex formation, were inhibited in vivo by A-tracts. Permanganate probing showed that the inhibition was accompanied by an A-tract-dependent accumulation of stalled initial transcribing complexes. A single A-tract was as effective as three. The phasing of the A-tracts with respect to the core promoter sequence was found to be important for promoter function. The position that caused maximal activation at one promoter caused maximal inhibition at another. These results suggest that the same molecular interaction gives rise to both inhibition and activation. This is likely to be due to facilitated RNA polymerase binding in the presence of A-tracts, which stimulates binding-limited promoters but inhibits promoter function in which polymerase escape and promoter clearance is rate limiting.
J
Mol
Biol 1994 Jun 17
PMID:Context-dependent effects of upstream A-tracts. Stimulation or inhibition of Escherichia coli promoter function. 800 62
Genetic linkage studies have indicated that chromosome 14q24.3 harbours a major locus for early-onset (onset age <65 years) Alzheimer's disease (AD3). Positional cloning efforts have identified a novel gene
S182
or presenilin 1 as the AD3 gene. We have mapped
S182
in the AD3 candidate region between D14S277 and D14S284 defined by genetic linkage studies in the two chromosome 14 linked, early-onset AD families AD/A and AD/B. We have shown that
S182
is expressed in lymphoblasts and have determined the complete cDNA in both brain and lymphoblasts by RT-PCR sequencing.
S182
is alternatively spliced in both brain and lymphoblasts within a putative phosphorylation site located 5' in the coding region. We identified two novel mutations, Ile143Thr and Gly384la located in, respectively, the second transmembrane domain and in the sixth hydrophilic loop of the putative transmembrane structure of
S182
. As families AD/A and AD/B have very similar AD phenotype our observation of two mutations in functionally different domains suggest that onset age and severity of AD may not be very helpful predictors of the location of putative
S182
mutations.
Hum
Mol
Genet 1995 Dec
PMID:Molecular genetic analysis of familial early-onset Alzheimer's disease linked to chromosome 14q24.3. 863 11
We report that expression of the somatostatin gene in pancreatic islets and in non-islet cells is negatively regulated by two proximal silencer elements,
PS1
and PS2. Transient transfection assays showed that
PS1
decreases somatostatin gene promoter activity stimulated by an upstream enhancer in the islet D-cell line RIN-1027-B2, but not in the islet B-cell line RIN-1046-38, whereas PS2 inhibits gene transcription both B- and D-cell lines. In BHK fibroblasts, both
PS1
and PS2 independently inhibit somatostatin gene in non-islet cells. DNA-binding studies revealed that both
PS1
and PS2 bind similar nuclear protein complexes in islet and non-islet cells (120 and 130 kDa).
PS1
also binds a 100-kDa protein present in islet B- and D-cell lines. In addition, both
PS1
and PS2 bind three D-cell-specific proteins (40, 43 and 45 kDa). These observations support a direct involvement of both positive and negative transcriptional control mechanisms in the regulation of the islet cell-specific expression of the somatostatin gene.
Mol
Cell Endocrinol 1995 Aug 30
PMID:Repression of somatostatin gene transcription mediated by two promoter silencer elements. 867 14
Missense mutations in the presenilin 2 (PS-2) gene on chromosome 1 were sought by direct nucleotide sequence analysis of the open reading frame of 60 pedigrees with familial Alzheimer's disease (FAD). In the majority of these pedigrees,
PS-1
and beta-amyloid precursor protein (beta APP) gene mutations had been excluded. While no additional PS-2 pathogenic mutations were detected, four silent nucleotide substitutions and alternative splicing of nucleotides 1338-1340 (Glu325) were observed. Analysis of additional members of a pedigree known to segregate a Met239Val mutation in PS-2 revealed that the age of onset of symptoms is highly variable (range 45-88 years). This variability is not attributable to differences in ApoE genotypes. These results suggest (i) that, in contrast to mutations in
PS-1
, mutations in PS-2 are a relatively rare cause of FAD; (ii) that other genetic or environmental factor modify the AD phenotype associated with PS-2 mutations; and (iii) that still other FAD susceptibility genes remain to be identified.
Hum
Mol
Genet 1996 Jul
PMID:Alzheimer's disease associated with mutations in presenilin 2 is rare and variably penetrant. 881 35
A positional cloning approach has led to the identification of two closely related genes, the presenilins (PS), for autosomal dominant presenile Alzheimer disease (AD):
PS-1
at 14q24.3 and PS-2 at 1q31-q42. The
PS-1
gene was identified by direct cDNA selection of yeast artificial chromosomes containing the candidate chromosomal region. Subsequently, the PS-2 gene was identified due to its high sequence homology with
PS-1
and its location within the candidate region defined by linkage studies. To date, 30 different missense mutations and one in-frame splice site mutation were described in
PS-1
, while only two missense mutations were detected in PS-2, suggesting that
PS-1
mutations are more frequently involved in familial presenile AD. The PS transcripts encode novel proteins that resemble integral transmembrane proteins of roughly 450 amino acids and at least seven transmembrane domains. The genomic organization of the PS genes is very similar showing that full length
PS-1
and PS-2 are encoded by 10 exons. However, different alternative splicing patterns have been observed for
PS-1
and PS-2 indicating that the corresponding proteins (ps-1 and ps-2) may have similar but not identical biological functions.
Hum
Mol
Genet 1996
PMID:The presenilin genes: a new gene family involved in Alzheimer disease pathology. 887 51
1
2
3
4
5
6
7
8
9
10
Next >>