Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regulatory wild-type locus sacU, which has a pleiotropic effect in Bacillus subtilis, notably on the synthesis of secreted proteins, was obtained from a colony bank of Escherichia coli harboring recombinant cosmids representative of the B. subtilis genome. It was shown that the sacU gene is located on a 2.4-kilobase KpnI-EcoRI fragment and that the cloned sequence is homologous to the corresponding chromosomal DNA fragment. The wild-type phenotype was recovered after transformation of SacU-, SacUh, and SacU- Rec- strains with the recombinant cosmid, indicating that the sacU locus has been cloned in totality. The sacU gene was expressed in a minicell-producing E. coli strain, and it was shown that it coded for a 46-kilodalton protein. In addition to the hypersecretion of proteins, SacUh mutants were characterized by the presence of a 46-kilodalton protein in the membrane fraction in higher amounts than were found in the wild-type strain. These mutants were also devoid of a 36-kilodalton polypeptide corresponding to the flagellin subunit. Analysis of the mRNA content of a secreted protein (levansucrase) in SacU- and SacUh mutants strongly suggested that the pleiotropic action of the sacU gene on the synthesis of levansucrase is exerted at a posttranscriptional level in B. subtilis cells and is probably correlated with the mechanism of secretion of exoenzymes.
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PMID:Cloning and expression in Escherichia coli of the regulatory sacU gene from Bacillus subtilis. 391 85

Crystals suitable for X-ray crystallographic investigation have been grown of several nucleic acid binding proteins and their analysis is in progress. These include E. coli catabolite gene activator protein (CAP), the large fragment of DNA polymerase I (Pol I fragment), rec A, single strand DNA binding protein, resolvase, lac repressor and lac repressor 'Core', 5S RNA fragment and its complex with L25. Calculation of the electrostatic charge potential of CAP, using coordinates refined at 2.6 A resolution, suggests an orientation for B DNA on this repressor and activator of transcription. Both the electrostatic calculations and detailed model building suggests that the DNA must be bent or kinked on the protein in this orientation in order to make sufficient protein contacts. From a 3.5 A resolution map of Pol I fragment we have been able to obtain a preliminary trace through the polypeptide backbone. The large fragment consists of two domains. The smaller domain binds nucleoside monophosphate at the edge of a mostly parallel beta-pleated sheet, a structure that is reminiscent of kinase and dehydrogenase nucleotide binding domains. The larger domain contains about two thirds of the fragment and is mostly alpha-helical but with at least one four stranded antiparallel beta-sheet. The nucleoside monophosphate binds with its 5' phosphate on the Mg and is apparently in the conformation of nucleotides in B DNA.
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PMID:Crystallographic studies of protein-nucleic acid interaction: catabolite gene activator protein and the large fragment of DNA polymerase I. 610 Oct 86

The cellular localization and regional distribution of insulin- and glucagonlike substance, C-peptide-like immunoreactivity, thiol:protein disulphide oxidoreductase, TPO (E.C.1.8.4.2.), and insulin/glucagon-specific proteinase, ISP (E.C.3.4.22.-), are studied in the CNS of man, adult and juvenile rats, mice, tortoises, and frogs by use of immunohistochemistry. Furthermore, the content of immunoreactive insulin, glucagon, and C-peptide was estimated in human cadaver brains by radioimmunoassay. It could be shown that insulinlike immunoreactive material is widely distributed in the human brain and the CNS of juvenile rats as well as in mice, whereas in the CNS of adult rats and nonmammalian animals (frogs, tortoises) the polypeptide is restricted to a few nerve cell populations. C-peptide immunoreactivity was demonstrated in human CNS in the same nerve cells as insulin. By use of two different glucagon-antisera it was revealed that gut-type glucagon occurs in many nerve cells of human and mouse brains, as well as in the CNS of juvenile rats. On the other hand, pancreas-type glucagon was less widely distributed in the human brain and nearly not detectable in the CNS of mice and rats. With the exception of neurosecretory nerve cells, there was a high degree of coincidence between the localization of insulin and TPO. The immunoreaction against the ISP antiserum was weak, but correlated well with the distribution of insulin-immunoreactivity. The occurrence of TPO and ISP in the brain demonstrates the ability of nervous tissue to degrade insulin and glucagon. By radioimmunoassay it was established that human brain contains insulin, glucagon and C-peptide at concentrations that exceed blood levels. We conclude from our data that, at least in part, cerebral insulin and glucagon are products of the brain itself.
Anat Rec 1983 Sep
PMID:Insulin- and glucagonlike peptides in the brain. 635 89

We are investigating the mechanisms for deletion formation through the use of mutants which alter deletion frequency together with well characterized systems for deletion detection. We report here on three mutations which were isolated for their ability to stimulate deletions in plasmid pMC874 (dli mutations). The mutation rec-2251 (formerly known as dli1) is a new allele of recBCD, a group of genes coding for the polypeptide components of the major recombination enzyme complex in E. coli; the second one, dli2 may be a new allele of uvrD, which codes for DNA helicase II; and the third one, dli3, has the phenotype of a mismatch repair mutation. Here we compare the effects of mutations in SOS-repair genes to those of the dli mutations on three different deletion events: (a) the deletion of short (60-100-bp) palindromic and non-palindromic inserts in derivatives of plasmid pBR325; (b) larger (600-800-bp) deletions in plasmid pMC874; and (c) the excision of the Tn10 transposon from chromosomal sites. Our results indicate that some form of SOS processing stimulates the loss of palindromes but not non-palindromes in plasmid pBR325 derivatives, and that RecA is necessary for UV-induced excision of Tn10 but this event is inhibited by UmuCD or its homolog MucAB. Each of the dli mutations showed unique effects on different classes of deletions. Mutation rec-2251 stimulated specifically deletions in pMC874 but had no effect on the deletion of non-palindromes in pBR325, and reduced the incidence of the other deletion events tested including loss of palindromic inserts in pBR325 as well as Tn10 excision. Mutation dli2, on the other hand, stimulated all deletions tested to varying extents, while dli3 did not affect markedly deletion formation in pBR325 plasmids but had a large stimulatory effect on both deletions in plasmid pMC874 and Tn10 excision. These results reveal that (a) some SOS-repair functions participate in deletion formation, (b) mutations selected for altering the incidence of one class of deletions may have totally different effects on other deletion events, and (c) the differences in mutant behavior may result in part from the ability of some pathways to discriminate among different deletion intermediates such as hairpins or cruciforms formed by palindromic sequences vs. transient secondary structures stabilized by direct repeats flanking non-palindromic sequences.
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PMID:Multiple pathways of deletion formation in Escherichia coli. 768 87

The pelvic flexure portion of the equine large colon is the proposed location of a pacemaker mechanism. This study was conducted to ascertain whether the distribution of certain putative neurotransmitters differs at the pelvic flexure compared to other sampling sites. Tissue samples were collected from the intestinal tracts of six horses. Serial sections from these samples were reacted with primary antisera specific for substance P, vasoactive intestinal polypeptide (VIP), methionine-Enkephalin, and calcitonin gene-related peptide (CGRP). The regional distribution of immunoreactive neuronal elements was uniform for each of the neuropeptides except VIP. Although neurons exhibiting VIP-like immunoreactivity were abundant throughout the colon, they were somewhat more plentiful near the apex of the pelvic flexure and the left dorsal colon. These neurons may participate in the initiation and propagation of the propulsive/retropulsive contraction waves, which emanate from this location and are believed to lend a sphincter-like capacity to the pelvic flexure. The submucosal plexus was replete with neurons with intense substance P and VIP-like reactivity. Reactive fibers left submucosal ganglia to project to the intestinal mucosa, reflecting a possible secretogogic role for these neurons. This role may be especially important for the horse as a hindgut fermenter. There were abundant methionine-Enkephalin and substance P-like reactive varicosities throughout the myenteric plexus, many of which established a pericellular plexus of varicose fibers. The abundance of these varicosities, which may correlate with a high degree of neuronal integration, did not vary regionally. These data may enhance our understanding of both normal colonic peristalsis and motility disorders caused by a depletion of these neuropeptides.
Anat Rec 1993 Jun
PMID:Neuropeptide distributions in the colon, cecum, and jejunum of the horse. 768 32

DNA sequencing, RNA mapping, and protein expression experiments revealed the presence of a gene, tfoX+, encoding a 24.9-kDa polypeptide, that is transcribed divergently from a common promoter region with the Haemophilus influenzae rec-1+ gene. H. influenzae strains mutant for tfoX failed to bind transforming DNA and were transformation deficient. Primer extension experiments utilizing in vivo total RNA from precompetent and competent H. influenzae cells demonstrated that transcription of tfoX+ increased immediately upon competence induction, suggesting that tfoX+ is an early competence gene. Similar experiments showed that the expression of the late competence-specific gene, com101A+, was tfoX+ dependent. Moreover, expression of plasmid-borne tfoX+ in H. influenzae resulted in constitutive competence. The addition of cyclic adenosine monophosphate (cAMP) to strains carrying a tfoX::lacZ operon fusion resulted in an immediate increase in beta-galactosidase activity that correlated with an increase in genetic transformability. Collectively, our results suggest that TfoX may play a key role in the development of genetic competence by regulating the expression of late competence-specific genes.
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PMID:Identification of a DNA transformation gene required for com101A+ expression and supertransformer phenotype in Haemophilus influenzae. 772 7

To study competence and the process of transformation (TFN) in pneumococci, we developed a method for isolating TFN- mutants using insertional inactivation coupled with fusions to the gene for alkaline phosphatase (phoA). One TFN- mutant transformed 2 log units less efficiently than the parent strain. Reconstitution of the mutated region revealed a locus, rec, that contains two polycistronic genes, exp10 and the previously identified recA (B. Martin, J. M. Ruellan, J. F. Angulo, R. Devoret, and J. P. Claverys, Nucleic Acids Res. 20:6412, 1992). Exp10 is likely to be a membrane-associated protein, as it has a prokaryotic signal sequence and an Exp10-PhoA fusion localized with cell membranes. On the basis of sequence similarity, pneumococcal RecA is a member of bacterial RecA proteins responsible for homologous recombination of DNA. DNA-RNA hybridization analysis showed that this locus is transcribed as a polycistronic message, with increased transcription occurring during competence. With an Exp10-PhoA chimera used as a reporter, there was a 10-fold increase in the expression of the rec locus during competence while there was only minimal expression under growth conditions that repressed competence. The TFN- mutant containing the exp10-phoA fusion produced activator, a small extracellular polypeptide that induces competence, and the expression of rec was induced in response to activator. Therefore, the rec locus is directly required for genetic transformation and is regulated by the cell signaling mechanism that induces competence.
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PMID:The rec locus, a competence-induced operon in Streptococcus pneumoniae. 779 54

Insulin-like growth factor I (IGF-I) is a 70 amino acid, mitogenic polypeptide, which, in mammals, acts through an endocrine, paracrine, and/or autocrine pathway to regulate growth and development. The primary goal of this study was to determine whether or not IGF-I-like immunoreactivity is present in the oviduct of the vitellogenic American alligator, Alligator mississippiensis, and if immunoreactivity patterns vary among the three functional oviducal regions: the albumen-secreting tube region, the anterior, fiber-secreting uterus, and the posterior, calcium-secreting uterus. Immunolocalization of IGF-I-like immunoreactivity was accomplished using a polyclonal antihuman rabbit antiserum with an immunoperoxidase staining system. IGF-I-like immunoreactivity was detected in all three oviducal regions of the vitellogenic alligator. The presence of IGF-I-like immunoreactivity in the oviduct suggests this hormone could function in the growth and proliferation of the alligator oviduct. Furthermore, the presence of IGF-I-like immunoreactivity in the tubal glands, which secrete components of the egg white, suggests that growth factors such as IGF-I may be synthesized by these glands and incorporated into the albumen during egg formation.
Anat Rec 1993 Aug
PMID:Localization of insulin-like growth factor-I-like immunoreactivity in the reproductive tract of the vitellogenic female American alligator, Alligator mississippiensis. 837 88

The expression of the complete human gastric lipase (HGL) gene in Saceharomyces cerevisiae grown in defined medium resulted in the secretion of active recombinant HGL (rec.HGL) to levels of up to approximately 11 mg/liter. Of the total measurable HGL activity, 90% was detected by assaying intact cells, suggesting that the majority of rec.HGL produced was secreted but stayed attached to the cell wall. The remaining 10% was present in the growth medium and from this source active rec.HGL was purified 300-fold by a combination of hydrophobic interaction and ion-exchange chromatography. Rec.HGL migrated on reduced SDS-PAGE as three bands with estimated molecular masses of 47,45, and 43 kDa. All three forms cross-reacted with an antibody raised to natural HGL and their treatment with Endo H showed them to be N-linked glycosylation variants of a single polypeptide. The 47-kDa species was isolated using lentil lectin Sepharose 4B and shown to possess a specific activity comparable to that of the natural enzyme. Rec.HGL had an acid pH activity optimum using either tributyrin or olive oil as substrate and did not lose activity if incubated in the presence of pepsin at pH 2.0. These results demonstrate that HGL secreted by Saccharomyces cerevisiae retained those properties of the natural enzyme required for its use in the treatment of pancreatic insufficiency.
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PMID:The secretion of active recombinant human gastric lipase by Saccharomyces cerevisiae. 886 Jun 47

Septation of the tubular heart to form the multi-chambered heart involves endocardial cell mesenchymal transformation at discrete sites. These sites include the crests of endocardial cushions at the atrioventricular junction, crests of the spiral ridges within the outflow tract, and the leading edge of the atrial septum. The factors involved in this multi-step inductive process appear to include the neural cell adhesion molecule (NCAM). The down-regulation of NCAM coincident with mesenchymal transformation has been documented at the atrioventricular cushion tissue. In view of the function-regulation properties of polysialylated NCAM (PSA-NCAM), we hypothesized that this form of NCAM would be playing a role during the dramatic changes in cell-cell interactions occurring in the endocardium at the leading edge of the primary atrial septum. Chicken hearts at stages during primary atrial septum development were fixed with paraformaldehyde and either immunofluorescently stained for the light microscope analysis or immunoperoxidase stained for ultrastructural analysis. A monoclonal antibody to an NCAM polypeptide epitope (5E) was used to detect all forms of NCAM, while a monoclonal to the polysialic acid (5A5) was used to detect that subset of NCAM which is highly polysialylated (PSA-NCAM). By light microscope level analysis, an increase in immunostaining for NCAM and the appearance of PSA-NCAM was detected on embryonic chicken endocardial cells at the leading edge of the growing atrial septum. The ultrastructural analysis revealed that there is also a change in the pattern of NCAM and PSA-NCAM from a polarized localization to a more ubiquitous distribution over the endocardial cell surface as these cells send out processes, form multiple layers, and sink or move into the underlying extracellular matrix. PSA-NCAM was also detected along cell appositions of cells within the matrix. Both NCAM and PSA-NCAM levels were reduced on cells deep within the matrix. These findings indicate that during primary atrial septation, PSA-NCAM may be deployed on endocardial epithelial cells in order to down-regulate cell-cell interactions and allow the detachment and migration of some of these cells into the underlying matrix.
Anat Rec 1997 01
PMID:Polysialylated NCAM expression on endocardial cells of the chick primary atrial septum. 898 5


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