Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SAM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2002

The SAM domain of polyhomeotic forms a helical polymer.

The polycomb group (PcG) proteins are important in the maintenance of stable repression patterns during development. Several PcG members contain a protein protein interaction module called a SAM domain (also known as SPM, PNT and HLH). Here we report the high-resolution structure of the SAM domain of polyhomeotic (Ph). Ph-SAM forms a helical polymer structure, providing a likely mechanism for the extension of PcG complexes. The structure of the polymer resembles that formed by the SAM domain of another transcriptional repressor, TEL. The formation of these polymer structures by SAM domains in two divergent repressors suggests a conserved mode of repression involving a higher order chromatin structure.

Amino Acid Motifs↗
PubMed2003

The RNA-binding SAM domain of Smaug defines a new family of post-transcriptional regulators.

Anteroposterior patterning in Drosophila melanogaster is dependent on the sequence-specific RNA-binding protein Smaug, which binds to and regulates the translation of nanos (nos) mRNA. Here we demonstrate that the sterile-alpha motif (SAM) domain of Smaug functions as an RNA-recognition domain. This represents a new function for the SAM domain family, which is well characterized for mediating protein-protein interactions. Using homology modeling and site-directed mutagenesis, we have localized the RNA-binding surface of the Smaug SAM domain and have elaborated the RNA consensus sequence required for binding. Residues that compose the RNA-binding surface are conserved in a subgroup of SAM domain-containing proteins, suggesting that the function of the domain is conserved from yeast to humans. We show here that the SAM domain of Saccharomyces cerevisiae Vts1 binds RNA with the same specificity as Smaug and that Vts1 induces transcript degradation through a mechanism involving the cytoplasmic deadenylase CCR4. Together, these results suggest that Smaug and Vts1 define a larger class of post-transcriptional regulators that act in part through a common transcript-recognition mechanism.

Amino Acid Sequence↗
PubMed1990

K-sam, an amplified gene in stomach cancer, is a member of the heparin-binding growth factor receptor genes.

DNA fragments amplified in a stomach cancer-derived cell line, KATO-III, were previously identified by the in-gel DNA renaturation method, and a 0.2-kilobase-pair fragment of the amplified sequence was subsequently cloned. By genomic walking, a portion of the exon of the gene flanking this 0.2-kilobase-pair fragment was cloned, and the gene was designated as K-sam (KATO-III cell-derived stomach cancer amplified gene). The K-sam cDNAs, corresponding to the 3.5-kilobase K-sam mRNA, were cloned from the KATO-III cells. Sequence analysis revealed that this gene coded for 682 amino acid residues that satisfied the characteristics of the receptor tyrosine kinase. The K-sam gene had significant homologies with bek, FLG, and chicken basic fibroblast growth factor receptor gene. The K-sam gene was amplified in KATO-III cells with the major transcript of 3.5-kilobases in size. This gene was also expressed in some other stomach cancer cells, a small cell lung cancer, and germ cell tumors.

Amino Acid Sequence↗
PubMed2001

Polymerization of the SAM domain of TEL in leukemogenesis and transcriptional repression.

TEL is a transcriptional repressor that is a frequent target of chromosomal translocations in a large number of hematalogical malignancies. These rearrangements fuse a potent oligomerization module, the SAM domain of TEL, to a variety of tyrosine kinases or transcriptional regulatory proteins. The self-associating property of TEL-SAM is essential for cell transformation in many, if not all of these diseases. Here we show that the TEL-SAM domain forms a helical, head-to-tail polymeric structure held together by strong intermolecular contacts, providing the first clear demonstration that SAM domains can polymerize. Our results also suggest a mechanism by which SAM domains could mediate the spreading of transcriptional repression complexes along the chromosome.

Amino Acid Sequence↗
PubMed1997

Age-related changes in the expression of Alzheimer's beta APP in the brain of senescence accelerated mouse (SAM)-P/10.

Patients with Alzheimer's disease (AD) show loss of memory and cognitive deficits the molecular mechanisms of which are not completely known. We examined age-related changes in the expression levels of beta-amyloid precursor protein (beta APP) in the brain of the senescence accelerated mouse (SAM) P/10, which shows age-dependent brain atrophy and impairment in learning and memory, and in the senescence resistant mouse (SAM)-R/1 using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Levels of both beta APP mRNA and protein increased with age, reaching a peak at 8 months of age in the hippocampus of SAM-P/10. In contrast, beta APP protein level decreased with age in the hippocampus of SAM-R/1 while beta APP mRNA level did not change significantly. Levels of beta APP mRNA and protein showed no change with ageing in other brain regions, including cerebral cortex, thalamus/midbrain and cerebellum brain stem. These results suggest that the beta APP over-expression in the hippocampus might be related to the characteristic memory loss in SAM-P/10.

Aging↗
PubMed1987

Histopathologic observations on the senescence-accelerated mice (SAM) reared under specific pathogen free conditions.

Five to 12 months old senescence-accelerated mice reared under specific pathogen free conditions (SPF SAM) were subjected to histopathologic examination. Senescence-prone SAM-P/1/Ta, P/3/Ta, and P/8/Ta exhibited marked depletion in thymic cortical lymphocytes which were associated with lymph follicle formation in the medulla, and marked infiltration of lymphocytes in the submaxillary gland, kidney, and other peripheral tissues. Morphometrical analysis of the adrenal gland revealed cortical atrophy and medullary hyperplasia in male SAM-P/8/Ta at 5 months of age. Other characteristic changes were marked vacuolation of the renal proximal tubules in male P/3/Ta and P/8/Ta mice, and degeneration of vascular wall in the testis of P/3/Ta mice. The pathogenesis of these changes appeared to be related to the adrenal lesions. Systemic amyloid deposition, one of the characteristic features of SAM housed in conventional facilities was not observed under the SPF condition. Acceleration of senescence in SPF SAM may arise from disorders of the thymus and adrenal.

Adrenal Glands↗
PubMed2004

1,25(OH)2D3 acts as a bone-forming agent in the hormone-independent senescence-accelerated mouse (SAM-P/6).

Recent studies suggest that vitamin D signaling regulates bone formation. However, the overall effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on bone turnover in vivo is still unclear. In this study, our aim was to examine the effect of 1,25(OH)2D3 on bone turnover in SAM-P/6, a hormone-independent mouse model of senile osteoporosis characterized by a decrease in bone formation. Male and female 4-mo-old SAM-P/6 mice were treated with 1,25(OH)2D3 (18 pmol/24 h) or vehicle for a period of 6 wk, and a group of age- and sex-matched nonosteoporotic animals was used as control. Bone mineral density (BMD) at the lumbar spine increased rapidly by >30 +/- 5% (P < 0.001) in 1,25(OH)2D3-treated SAM-P/6 animals, whereas BMD decreased significantly by 18 +/- 2% (P < 0.01) in vehicle-treated SAM-P/6 animals and remained stable in control animals during the same period. Static and dynamic bone histomorphometry indicated that 1,25(OH)2D3 significantly increased bone volume and other parameters of bone quality as well as subperiosteal bone formation rate compared with vehicle-treated SAM-P/6 mice. However, no effect on trabecular bone formation was observed. This was accompanied by a marked decrease in the number of osteoclasts and eroded surfaces. A significant increase in circulating bone formation markers and a decrease in bone resorption markers was also observed. Finally, bone marrow cells, obtained from 1,25(OH)2D3-treated animals and cultured in the absence of 1,25(OH)2D3, differentiated more intensely into osteoblasts compared with those derived from vehicle-treated mice cultured in the same conditions. Taken together, these findings demonstrate that 1,25(OH)2D3 acts simultaneously on bone formation and resorption to prevent the development of senile osteoporosis.

Absorptiometry, Photon↗
PubMed1996

Genetic analysis of the sam mutations, which induce sexual development with no requirement for nutritional starvation in fission yeast.

The cAMP pathway and the Ras pathway are the two major pathways to sexual development in the fission yeast Schizosaccharomyces pombe. To understand the cAMP pathway or the related pathway, we analyzed mutants that display a phenotype similar to cyr1-, that is, hyper-sporulation. Nine mutants termed sam (sporulation abnormal mutant), which are highly inclined to sexual development despite the presence of nitrogen sources, were partially characterized. Cyclic AMP was detected in all nine sam mutant cells, and over-expression of the adenylyl cyclase gene (cyr1) failed to suppress the hyper-sporulation phenotype of these sam mutants, suggesting that none of the sam mutants were likely to be allelic to cyr1. Epistatic tests of sam mutants showed that they were divided into two dominant and seven recessive mutants. Dominants were able to make spores in sam/sam+ heterodiploid cells upon abundant nutrients. Both two dominant mutants bypassed the inability to make spores in ras1 deficient diploid cells, suppressed the deficiency to execute sporulation in byr2 deficient diploid cells, but failed to suppress the byr1 deficiency. Two dominant mutations seem not to occur within the byr2 gene.

Base Sequence↗
PubMed1997

A gene homologous to the Streptomyces chymotrypsin-like protease (SAM-p20) gene is tandemly located.

A gene encoding a homolog of the Streptomyces chymotrypsin-like serine protease, SAM-P20, was identified downstream of the sam-p20 gene and designated SAM-P20D. This gene has two tandem Shine Dalgarno sequences and two initiation codons. We have established vector systems with the function of tyrosinase gene-bone melanin pigmentation as a reporter for sam-p20D gene expression in Streptomyces coelicolor in order to identify the promoter and terminator activities. Using this system, the sam-p20D gene was suggested to be transcribed monocistronically.

Amino Acid Sequence↗
PubMed2002

Sinobronchial allergic mycosis: the SAM syndrome.

We contend that the presence of concomitant allergic fungal sinusitis (AFS) and allergic bronchopulmonary mycosis in the same patient represents an expression of the same process of fungal hypersensitivity in the upper and lower airways. We have termed this process the SAM syndrome, an acronym for sinobronchial allergic mycosis. Diagnostic criteria have been established for the SAM syndrome, and the clinical characteristics of one previously unreported and four previously reported patients have been tabulated. Patients with the SAM syndrome have chronic sinusitis involving multiple sinuses, asthma, immediate cutaneous reactivity to fungal allergens, peripheral eosinophilia, and radiographic evidence of bronchiectasis. Total serum IgE levels are usually elevated as well. A variety of chest radiographic abnormalities may occur, ranging from mass lesions to diffuse pulmonary infiltrates and even normal findings on chest radiographs. Patients present for an evaluation of either sinus or lung disease and, at that time, demonstrate no clinical features that distinguish them from patients with isolated sinus or lung disease. All patients reported to date have had clinical responses to therapy with corticosteroids. We postulate that SAM is underdiagnosed in patients with AFS, a disease recently reported from medical centers in the southeastern and western United States. Moreover, since our patient had a mutation in the cystic fibrosis transmembrane conductor regulator (CFTR) gene, we further hypothesize that CFTR gene mutations may play an important role in the pathogenesis of the SAM syndrome.

Adolescent↗
PubMed2005

Structural and functional comparison of HemN to other radical SAM enzymes.

Radical SAM enzymes have only recently been recognized as an ancient family sharing an unusual radical-based reaction mechanism. This late appreciation is due to the extreme oxygen sensitivity of most radical SAM enzymes, making their characterization particularly arduous. Nevertheless, realization that the novel apposition of the established cofactors S-adenosylmethionine and [4Fe-4S] cluster creates an explosive source of catalytic radicals, the appreciation of the sheer size of this previously neglected family, and the rapid succession of three successfully solved crystal structures within a year have ensured that this family has belatedly been noted. In this review, we report the characterization of two enzymes: the established radical SAM enzyme, HemN or oxygen-independent coproporphyrinogen III oxidase from Escherichia coli, and littorine mutase, a presumed radical SAM enzyme, responsible for the conversion of littorine to hyoscyamine in plants. The enzymes are compared to other radical SAM enzymes and in particular the three reported crystal structures from this family, HemN, biotin synthase and MoaA, are discussed.

Atropine Derivatives↗
PubMed1999

Deletion of the carboxyl-terminal exons of K-sam/FGFR2 by short homology-mediated recombination, generating preferential expression of specific messenger RNAs.

The K-sam gene was first identified as an amplified gene from human gastric cancer cell line KATOIII, and its product is identical to fibroblast growth factor receptor 2. The K-sam gene is located on human chromosome 10q26 and is preferentially amplified in the poorly differentiated types, especially in the scirrhous type, of gastric cancers. During the course of studies on the structural characterization of the amplification units, we found that the carboxyl-terminal exons of K-sam were deleted in three of four of the scirrhous type of gastric cancer cell lines. These deletions generate preferential expression of mRNAs encoding K-sam proteins lacking the carboxyl-terminal region containing the tyrosine residues at positions 780, 784, and 813. The carboxyl-terminal region has been reported to have a sequence required for the inhibition of NIH3T3 transformation, indicating that cells with amplification of the truncated K-sam gene have a growth advantage during the carcinogenic process for the scirrhous type of gastric cancers. This is the first report showing the deletion of the carboxyl-terminal exons of the receptor-type of the protein tyrosine kinase gene. Sequence analysis of the DNA sequences surrounding the deletion junctions shows the presence of unique sequences and indicates the involvement of short homology-mediated recombination in the generation of these deletions.

3T3 Cells↗
PubMed2000

Blood viscosity and red cell morphology in subjects suffering from cirrhosis before and after treatment with S-adenosyl-L-methionine (SAM).

Alterations of fluidity of the hepatocytic membrane and of the transport related systems are the basis of the cholesteatic syndrome and favour the tissue accumulation of cytotoxic metabolites. S-Adenosyl-L-Methionine (SAM) is a natural molecule which acts as a giver of methylic groups and as an enzymatic activator in several enzymatic actions of transmethylase and of transulphuration and plays a key role in biochemical processes of hepatic cell. The aim of our study was to evaluate the effects of SAM on the restoration of the membrane fluidity and on the hepatic function in general. In studying the fluidity of the cell membrane we evaluated some hemorheological parameters (total blood viscosity and red cell morphology). Fluidity of the red cell membrane is one of the most important elements of red cell rheology. We studied 15 patients (Group A) suffering from micro- and macro-nodular cirrhosis verified through hepatic biopsy, with alcoholic or post-viral causes. We evaluated the values of: blood viscosity (with a cone-plate rheometer by Carri-med), haematocrit, plasma fibrinogen and the erythrocytic morphology at the optical microscope with the Zipursky-Forconi method before and after 7 days of therapy with SAM i.v.. Data were compared with those of a similar group (Group B) treated with traditional therapy only (hyposodic and hypoprotein diet supplemented with multivitamin preparations, vitamin K in particular, if necessary, and potassium sparing diuretics). We also measured biliary salts, alkaline phosphatase, transaminase and gamma-GT. In the first group we observed a statistically significant reduction of blood viscosity, haematocrit didn't change significantly; biliary salts reduced in a statistically significant way. Evaluation of red cell morphology showed in all cases a pathological percentage (>15%) of echinocytes and knizocytes which reduced to a mean of 5% after SAM therapy. We observed no further modifications of the other hemorheological parameters. Results demonstrate that SAM has a positive action on the fluidity of the membrane, as indicated by the improvement of haemorheological parameters and by the significant decrease of biliary salts, indicating the presence of cholesteasis.

Blood Viscosity↗
PubMed2002

[Production of SAM by recombinant Pichia pastoris].

To utilize Pichia pastoris to produce S-adenosyl-L-methionine (SAM), an intracellular expression vector harboring S. cerevisiae SAM2 was transformed into GS115. A recombinant strain having 2 copies of expression cassette was obtained through G418 resistance screening. This strain had higher SAM synthetase activity and higher SAM production capacity than the original strain, when cultured in medium containing methanol and methionine. The carbon source and nitrogen source of medium was optimized. The results showed SAM production by this strain was closely related to carbon metabolism. With supplementation of 0.2% glycerol every day from the beginning of 3rd day, this strain produced 1.58 g/L SAM when cultured in a medium containing 0.75% L-methionine and optimized carbon and nitrogen source after 6 days.

Methionine Adenosyltransferase↗
PubMed1992

Age-related changes in GSH content of eyes in mice--a comparison of senescence-accelerated mouse (SAM) and C57BL/J mice.

1. Age-related changes in glutathione (GSH) content of eye lenses were investigated in senescence-accelerated mouse (SAM) and C57BL/J mice. 2. The decrease of GSH content with aging is markedly observed in SAM strains. 3. The oxidized glutathione (GSSG) content of eyes increased significantly with aging in SAM. 4. Ophthalmic changes, including cataract, increased with age in SAM alone. 5. The decrease of GSH content and the increase of GSH oxidation may be involved in the pathogenesis of cataract in SAM.

Aging↗
PubMed1979

[Transient systolic anterior movement of the mitral valve (SAM) without asymmetric septal hypertrophy (case report with post-mortem examination) (author's transl)].

Typical SAM of the mitral valve was detected by echocardiography in a 71-year-old patient with acute myocardial infarction. The patient showed auscultation signs of IHSS and was digitalized and hypovolemic secondary to diarrhea. Following rehydration and digitalis being discontinued, SAM was no longer seen. There were no signs of IHSS at post-mortem examination. This case demonstrates that obstruction of left ventricular outflow tract together with echocardiographical findings of SAM and the typical clinical signs of IHSSS may be observed without the presence of asymmetric septal hypertrophy. This supports the hypothesis that ejection dynamics in a small and asynergically contracting left ventricle may contribute substantially to the appearance of SAM. On the other hand echocardiographic findings of SAM without asymmetric septal hypertrophy may not exclude symptoms of IHSS.

Aged↗
PubMed1991

Immune responses in newly developed short-lived SAM mice. IV. Chromosomal location of a gene controlling defective helper T-cell activity.

Short-lived SAMP-P/1 mice are low responders in in vitro antibody responses because of a selectively impaired helper T(Th)-cell activity. After crossing with high responders (B10.BR mice), about 12% of (B10.BR x SAM-P/1) (BRP)F2 mice showed low responsiveness, as did SAM-P/1 mice, against two T-dependent antigens, sheep and horse red blood cells (RBC), both of which were not cross-reactive to each other at helper T- and B-cell levels. The immune activities against the two antigens in individual BRPF2 mice showed a good correlation (r = 0.81), thereby suggesting that SAM-P/1 mice have an antigen non-specific Th cell dysfunction. Based on the incidence of the low responders in F2 generation and statistical analyses, the hypo-responsiveness was postulated to be controlled by two genes. To survey the location of these genes, linkage analyses were performed in the F2 mice using a large set of genetic markers. Low responders in the F2 generation showed a significantly higher incidence of SAM-P/1 genotype at the Gpi-1 as well as c locus on chromosome 7 (Chr.7). However, no linkage of low responsiveness to the Hbb locus was evident, an area present at a more distal site to the centromere on the same chromosome. These results suggest that one of the genes controlling the hypo-responsiveness of SAM-P/1 mice is linked to both Gpi-1 and c loci and that it locates at a more proximal site on Chr.7.

Animals↗
PubMed1989

Lung derived surface active material (SAM) inhibits natural killer cell tumor cytotoxicity.

Natural killer cells have been identified in lung tissue but have been found to have significantly less tumor cytotoxicity than natural killer cells found elsewhere in the body. The natural killer cells in the lung are still functional, since their killing can be enhanced by Interleukin-2. The surface active material (SAM) of lung lining fluid has been shown to have immunomodulating activity, including the suppression of lymphocyte blast transformation and enhancement of macrophage tumor cytotoxicity. We studied the effect of SAM purified from lung lining fluid on natural killer cell tumor cytotoxicity. SAM markedly inhibited tumor killing (Percent cytotoxicity of cells alone: 41 +/- 7.3% (mean +/- SEM); cells plus SAM: 10 +/- 9.7%, p less than 0.02). Further studies demonstrated that some phospholipids, including phosphatidylcholine, the major phospholipid of SAM, also significantly inhibited natural killer cell tumor killing. This inhibition of natural killer cell tumor cytotoxicity could be reversed by the addition of Interleukin-2 to the natural killer cells. These studies demonstrated that the surfactant found in lung lining fluid significantly inhibited natural killer cell tumor cytotoxicity and this effect could be reversed by Interleukin-2.

Cytotoxicity, Immunologic↗