PubMed HealthSearch

SEARCH · PubMed Health

Results for “Subcellular localization”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 37 records · Page 2Linked to original sources

Phenylalanine 347 regulates the subcellular localization of PTEN.

PTEN plays diverse tumor-suppressive roles, including inhibition of PI3K-AKT signaling and maintenance of genomic integrity in the nucleus. Elucidating the molecular mechanisms regulating its subcellular localization is therefore essential for understanding PTEN functions. PTEN350, a fragment comprising the N-terminal phosphatase and C2 domains of PTEN, preferentially localizes to the nucleus, although the residues responsible for this localization remain unclear. Previously, we demonstrated that Thr348 contributes to the prominent nuclear accumulation of the PTEN350 fragment and PTENA4 carrying alanine substitutions in the Ser380/Thr382/Thr383/Ser385 (STTS) motif. Since our previous findings suggested that Phe347 also contributes to PTEN nuclear localization, we investigated its role in the present study. Phe347 substitutions (F347A, F347Y, and F347L) were introduced into PTEN and its mutant or truncated derivatives, including PTEN350, PTEN, PTENA4, PTEN350,K13R, and PTENK13R,A4, either alone or in combination with T348D. The F347A substitution significantly attenuated the nuclear accumulation of PTEN350 and PTENA4, whereas F347L partially preserved nuclear accumulation and F347Y substitution exhibited an intermediate phenotype. Similar effects of the F347 substitutions were also observed in the T348D mutants, although the differences among the three substitutions were less pronounced. A similar pattern was observed for the plasma membrane localization of PTEN350,K13R and PTENK13R,A4, with F347A causing the greatest reduction, F347L retaining partial membrane localization, and F347Y exhibiting an intermediate phenotype. The effects of these substitutions were consistently observed in both HEK293T cells and HeLa cells. Collectively, these findings indicate that Phe347 is an important determinant of PTEN subcellular localization.

Nuclear translocation

Subcellular localization of gamma-glutamyltransferase in calf thymocytes.

The subcellular localization of gamma-glutamyltransferase in calf thymocytes was investigated and compared with that of alkaline phosphodiesterase I, alkaline nitrophenyl phosphatase, succinate-tetrazolium oxidoreductase (succinate-INT reductase) and lactate dehydrogenase after two different methods of cell disruption and differential centrifugation. Most of the activity was recovered in the crude membrane fractions (43.0%), but significant amounts co-pelleted with the large-granule (mitochondria) fractions (31%). The specific activity of the gamma-glutamyltransferase in the purified plasma membrane was 30-50 times that of the enzyme in the cell homogenate and had a similar subcellular distribution to the plasma-membrane markers, alkaline phosphodiesterase I and alkaline nitrophenyl phosphatase. It was concluded that gamma-glutamyltransferase was primary a plasma-membrane-bound enzyme, and that its location in other subcellular fractions was probably due to their contamination with plasma-membrane vesicles.

Animals

Subcellular localization and release of human neutrophil gelatinase, confirming the existence of separate gelatinase-containing granules.

An e.l.i.s.a. was developed using specific polyclonal rabbit antibodies against human neutrophil gelatinase. This assay, in contrast to the functional assay, is independent of activation of gelatinase, and is specific for the detection of gelatinase in both its reduced and unreduced forms. Using this assay, we were able to demonstrate a difference between the subcellular localization of gelatinase on the one hand, and the subcellular localization of vitamin B-12-binding protein, lactoferrin and cytochrome b558 on the other hand. The latter three co-localized in fractions of slightly higher density than gelatinase on a two-layer Percoll density gradient. Furthermore, the release of gelatinase exceeded the release of vitamin B-12-binding protein as well as lactoferrin by a factor of 3-6 following stimulation with formylmethionyl-leucyl-phenylalanine, leukotriene B4 and other soluble stimuli. Thus, although gelatinase has previously been found to co-localize with lactoferrin on immuno-electron microscopy, we confirm the existence of gelatinase-rich and lactoferrin- and vitamin B-12-binding-protein-poor granules, that are lighter and mobilized more easily than specific granules. These gelatinase-containing granules are not the store of cytochrome b558.

Cytoplasmic Granules

Nonspecific lipid transfer protein in castor bean cotyledon cells: subcellular localization and a possible role in lipid metabolism.

The subcellular localization and several biochemical activities of nonspecific lipid transfer protein (nsLTP) were investigated. A section of a castor bean cotyledon cell was labeled with anti-nsLTP serum followed by protein A-gold. Gold particles were more abundant in the glyoxysome matrix and the vessel cell wall than in other areas. Cell fractionation analysis of 6-day-old castor bean cotyledons by sucrose density gradient centrifugation demonstrated that 13% of nsLTP was distributed in the glyoxysomal fraction, identified on the basis of catalase as a marker, and 87% in the soluble fraction near the top of the gradient. The location of castor bean nsLTP in glyoxysomes was further confirmed by in vitro import experiments. The synthesized precursor of nsLTP (pro-nsLTP-C) was incorporated into intact castor bean glyoxysomes and processed to the mature form after import into the glyoxysomes, but it was not imported into canine pancreatic microsomes. Castor bean nsLTP-A was found to possess the ability to bind oleic acid and oleoyl-CoA by means of a method involving Lipidex 1000. The dissociation constants (Kd) for oleic acid and oleoyl-CoA binding to nsLTP-A were 4.8 and 5.0 microM, respectively. The saturated binding capacities (Bmax) for oleic acid and oleoyl-CoA per mol of nsLTP-A were 1.1 and 1.2 mol, respectively. When acyl-CoA oxidase activity was assayed in the glyoxysomal fraction, marked enhancement of the activity was observed in the presence of nsLTP. These results suggest the possibility that nsLTP regulates fatty acid beta-oxidation through the enhancement of acyl-CoA oxidase activity in glyoxysomes. The occurrence of castor bean nsLTP in the vessel wall was discussed.

Acyl Coenzyme A

Acyl-CoA oxidase, peroxisomal thiolase and dihydroxyacetone phosphate acyltransferase: aberrant subcellular localization in Zellweger syndrome.

We have studied the presence and subcellular localization of peroxisomal 3-oxoacylcoenzyme A thiolase, acylcoenzyme A oxidase and acyl-CoA: dihydroxyacetonephosphate acyltransferase (DHAPAT) in fibroblasts from control subjects and patients with an inherited deficiency of peroxisomes (Zellweger syndrome), using immunofluorescence spectroscopy and density gradient centrifugation techniques. The results show that Zellweger cells contain unprocessed thiolase and unprocessed acyl-CoA oxidase which are associated with structures containing a peroxisomal integral membrane protein of 69 kDa and having a density much lower than that of normal peroxisomes. The residual DHAPAT activity present in Zellweger cells is also contained in these structures. We conclude that these structures represent defectively assembled peroxisomes which may still be capable of importing some peroxisomal proteins.

Acetyl-CoA C-Acetyltransferase

Subcellular localization of enterokinase (enteropeptidase EC 3.4.21.9) in rat small intestine.

The subcellular localization of enterokinase is controversial. In this study, enterokinase was extracted from a soluble fraction and a brush border fraction of rat small intestine by differential centrifugation. The soluble fraction contained 41% of the initial enterokinase activity while the brush border fraction contained only 4.6% of the initial activity. In contrast, alkaline phosphatase monitored as a brush border marker, yielded 26.3% in the brush border fraction and only 6% in the soluble fraction. Further separation of the soluble fraction on a Sepharose 4B column revealed three peaks of enterokinase activity. One small peak (3%) of a bound enzyme (Mr, 2 - 10(6)) and two larger peaks of free enzyme (Mr, 3 - 10(5) and 9 -10). In contrast, alkaline phosphatase major fraction was in a high molecular weight peak of bound enzyme. When the brush border fraction was chromatographed only a single peak of bound enterokinase and alkaline phosphatase were found. In the lower part of the small intestine, no brush border-bound enterokinase was found, while the peak of alkaline phosphatase was the same as in the upper intestine. These data suggest that enterokinase activity in the rat intestine is mainly in a free form localized in the mucin and soluble fraction and to a negligible extent in the brush border.

Alkaline Phosphatase

[Subcellular localization of glutamine synthetase activity in carp muscle tissue and liver].

Subcellular distribution of the glutaminesynthetase activity (EC 6.3.1.2) is studied in muscle tissue and liver of carp. It is established that this activity is distributed by subcellular fractions analogously to the glutamatedehydrogenase activity--enzyme-marker activity of mitochondria. An additional evidence for the association of the two given enzymes is obtained during equilibrium density-gradient centrifugation of mitochondria on 30-60% gradient of sorbitol. Comparison of the obtained results with data from literature testifies to a coincidence of the subcellular localization of the processes of ammonia formation and binding into glutamine, thus confirming a view of the leading role of glutaminesynthetase in ammonia detoxication in carps.

Ammonia

Subcellular localization and heterogeneity of neutral proteases in neutrophilic polymorphonuclear leukocytes.

The subcellular localization of elastase and of neutral proteases hydrolyzing histone and casein was determined in human and rabbit polymorphonuclear leukocytes using fractionation by isopycnic centrifugation. Granule-rich fractions obtained by this technique were extracted and analyzed by acrylamide gel electrophoresis, and proteolytic activity on the gels was demonstrated by staining with either N-acetyl-D,L-alanine alpha-naphthyl ester or naphthol AS-D acetate as substrate. In both species, all neutral proteases assayed were found to be localized exclusively in the azurophil granules. Specific activities were about 10-30 times higher in human than in rabbit preparations. In extracts of human azurophil granules up to 10 proteins exhibiting esterolytic activity could be demonstrated after electrophoretic separation. Three major and two or three minor components of these esterases were shown to possess elastase activity. Similar zymograms prepared with extracts from rabbit azurophil granules revealed only one major elastase band. The electrophoretic analysis further showed that the most strongly cationic proteins of both human and rabbit PMNs were also confined to the azurophil granules.

Alkaline Phosphatase

Subcellular localization and binding of 125I-triiodothyronine in calf thyroid.

The subcellular distribution of 125I-T3 was studied in calf thyroid slices, under the same experimental conditions where T3 inhibits protein and RNA synthesis, labelled hormone was found mainly in the 20,000 X g supernatant. The specificity of each subcellular localization was determined by incubating the slices with 10(-5)M T3. Only in the purified nuclei a significant decrease was found, indicating a specific localization of the labelled hormone. When slices were incubated with 125I both labelled T3 and T4 were found in purified nuclei, indicating that endogenously synthesized hormones can reach thyroid nuclei. Purified thyroid nuclei were incubated with labelled T3 and increasing amounts of cold hormone. Specific binding reached a plateau after 90 min of incubation at 20 degrees C. When the displacement curves were analysed by a Scatchard plot a binding site with a Ka of 5.2 X 10(7) M-1 and a capacity of 3.0 X 10(-15) moles/microgram DNA was observed. Digestion of nuclei with trypsin and protease abolished completely the binding of 125I-T3 thus indicating the protein nature of the receptor. The hormone-receptor complex could be extracted with 0.4M KCI and eluted in the void volume after Sephadex G-25 column chromatography, similar to peripheral tissues nuclear T3 receptors. The present studies provide the first evidence for the existence of nuclear receptors for T3 in the thyroid, an event probably related to the autoregulatory mechanism.

Animals

Subcellular localization and partial characterization of bovine corpus luteum adenylate cyclase.

The subcellular localization of adenylate cyclase (ATP pyrophosphatelyase (cyclizing), EC 4.6.1.1) in bovine corpus luteum was studied using isotonic and hypotonic homogenization and fractionation conditions. All fractions prepared were assayed for adenylate cyclase, marker enzymes and DNA. Only plasma membrane marker enzyme, 5'-nucleotidase paralleled the distribution of adenylate cyclase under both isotonic and hypotonic conditions (conditionsoth isotonic and hypotonic conditions (coefficient of correlation = 0.95). Two main fractions prepared under hypotonic conditions were subfractionated by discontinuous sucrose gradient centrifugation. The highest amount of adenylate cyclase was found in a fraction having a density approximately equal to 1.13 g/cm3. The specific activity of this fraction was 4--6 times higher than that of the homogenate. The electron microscopic study of this fraction revealed the presence of a single type of particulate material consisting of small vesicles exhibiting a typical unit membrane structure. It is concluded that this adenylate cyclase is primarily localized in the plasma membranes. Basal adenylate cyclase activity of plasma membranes was stimulated 2--3 times by luteinizing hormone (10 mug/ml), 3--4 times by prostaglandin E2 (10 mug/ml), 4--6 times by NaF (0.01 M) and two times by methanol (0.2%).

Adenylyl Cyclases

Subcellular localization of ferritin and iron taken up by rat hepatocytes.

The subcellular localization of ferritin and its iron taken up by rat hepatocytes was investigated by sucrose-density-gradient ultracentrifugation of cell homogenates. After incubation of hepatocytes with 125I-labelled [59Fe]ferritin, cells incorporate most of the labels into structures equilibrating at densities where acid phosphatase and cytochrome c oxidase are found, suggesting association of ferritin and its iron with lysosomes or mitochondria. Specific solubilization of lysosomes by digitonin treatment indicates that, after 8 h incubation, most of the 125I is recovered in lysosomes, whereas 59Fe is found in mitochondria as well as in lysosomes. As evidenced by gel chromatography of supernatant fractions, 59Fe accumulates with time in cytosolic ferritin. To account for these results a model is proposed in which ferritin, after being endocytosed by hepatocytes, is degraded in lysosomes, and its iron is released and re-incorporated into cytosolic ferritin and, to a lesser extent, into mitochondria.

Animals

Studies of dihydroxyacetone phosphate acyltransferase in rat small intestine. Subcellular localization and effect of partially hydrogenated fish oil and clofibrate.

The subcellular localization of dihydroxyacetone phosphate acyltransferase (DHAPAT) activity in rat small intestine was investigated by Nycodenz-gradient centrifugation. We found that DHAPAT had a predominant peroxisomal distribution, with a separate enzyme activity located in the microsomal fraction, the same distribution as found in rat liver. The effect of feeding rats on a diet with 20% (w/w) partially hydrogenated fish oil (PHFO) or 0.3% clofibrate on the activity of DHAPAT in rat small intestine and liver was studied. Both 20% PHFO and 0.3% clofibrate gave a 1.8-fold stimulation of the specific activities of DHAPAT in peroxisomes of the small intestine, whereas in the liver 20% PHFO gave a 1.4-fold stimulation and 0.3% clofibrate a 1.6-fold stimulation of the total DHAPAT activities in the postnuclear supernatant. The specific activities of DHAPAT in liver were not affected.

Acyltransferases

Subcellular localization of glutamate dehydrogenases and alanine aminotransferase in epimastigotes of Trypanosoma cruzi.

The subcellular localization of NAD- and NADP-linked glutamate dehydrogenases (GDH-NAD and GDH-NADP), alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) in epimastigotes of Trypanosoma cruzi was studied by digitonin extraction from whole cells, subcellular fractionation by differential centrifugation and isopycnic ultracentrifugation. All enzymes presented both a cytosolic and a mitochondrial form; in addition, GDH-NADP seems to have a third, still undefined, localization. The results are compatible with the existence of two pathways for the production of L-alanine linked to the reoxidation of glycolytic NADH, one operative in the mitochondrion and the other in the cytosol, and perhaps responsible for the existence of the two alanine pools detected by 13C-nuclear magnetic resonance (B. Frydman et al., Eur. J. Biochem. 192 (1990) 363-368).

Alanine Transaminase

Subcellular localization of a thromboxane A2/prostaglandin H2 receptor antagonist binding site in human platelets.

The subcellular localization of a binding site for the competitive thromboxane A2/prostaglandin H2 (TXA2/PGH2) antagonist, 9,11-dimethylmethano-11,12-methano-16-(3-iodo-4- hydroxyphenyl)-13,14-dihydro-13-aza-15 alpha beta-omega-tetranor TXA2 ([125I]-PTA-OH), was determined. Subcellular fractions of platelets were prepared by glycerol lysis or nitrogen cavitation, and were characterized by the use of enzymatic markers specific for plasma membranes, endoplasmic reticulum (dense tubular system), mitochondria, granules, and cytosolic constituents. The Kd and density of binding sites in the subcellular fractions were determined by Scatchard analysis of equilibrium binding data. The Kd and Bmax for [125I]-PTA-OH determined in the lysates were 49 +/- 11 nM and 4.1 +/- 1.7 pmol/mg protein respectively (N = 6). The Kd values were not significantly different in any of the fractions assayed. The binding sites were coenriched (4.5 +/- 0.66 fold) with the enzymatic markers for plasma membranes (3.7 +/- 0.5 fold) and dense tubular system (2.4 +/- 0.4 fold). The binding sites were not coenriched with markers for cytoplasmic constituents, mitochondria, or granules. The ability of the TXA2/PGH2 mimetic U46619 to compete with [125I]-PTA-OH for the binding site was also determined for the various subcellular fractions. The IC50 for U46619 was 5.4 +/- 1.2 microM in the lysate, and was not significantly different in the subcellular fractions. These data suggest that the binding site is the TXA2/PGH2 receptor described previously. These data are consistent with the notion that the putative TXA2/PGH2 receptor is localized in the plasma membranes and/or the dense tubular system.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5

Subcellular localization of three degeneration-associated phospholipids in cultured hamster fibroblasts (BHK21 cells).

Subcellular localization of bisphosphatidic acid, semilysobisphosphatidic acid and phosphatidyl-(N-acyl)ethanolamine was studied in normal and degenerating fibroblasts (BHK21 cells) by differential centrifugation. In the normal cells these lipids were highly enriched in the floating fraction consisting mainly of neutral lipid-rich lysosomes. They were also enriched in the mitochondrial fraction. In degenerating cells the high enrichment in the floating fraction was retained, but the other peak was displaced to the crude nuclear fraction. Subfractionation of the crude nuclear fraction indicated that these lipids were not enriched in the purified nuclei. Instead, their concentrations were relatively high in the other subfraction evidently enriched in the large secondary lysosomes characteristic for the degenerating cells. Neither in normal nor degenerating cells were these lipids enriched in the light mitochondrial fraction, where most of the smaller, and probably younger, lysosomes were found. On the basis of these results it is suggested that bisphosphatidic acid, semilysobisphosphatidic acid and phosphatidyl-(N-acyl)ethanolamine are lysosomal in origin. It appears possible that they are specifically associated with the organelles representing the later stages in the lysosomal lifespan.

Animals

Cellular and subcellular localization of 3h-diethylstilboestrol in the central nervous system.

The cellular and subcellular localization of radioactivity in the brain of immature female rats was determined by dry-mount autoradiography 2 h after iv injection of 1.0 microgram of (monethyl-3H) diethylstilboestrol per 100 g body weight. A specific topographic pattern of nuclear concentration of the synthetic oestrogen was obtained similar to that for 3H-oestradiol-17 beta in specific neurons of the basal hypothalamus, preoptic region and amygdala. In competition experiments, the nuclear concentration of radioactivity in all areas studied was inhibited by unlabeled oestradiol, while unlabeled testosterone had no effect. These data suggest that although oestradiol can bind to androgen receptors, the oestrogen receptor itself can account for the localization seen after the injection of 3H-oestradiol.

Amygdala

Subcellular localization of blood group substances ABH in human salivary glands.

We investigated the subcellular localization of ABH antigens in human submandibular, sublingual, and buccal glands by applying a post-embedding immunogold method using monoclonal antibodies specific for A, B, and H antigens. In most glands the immunoreactivity was usually restricted to mucous cells, in which only secretory granules and sometimes Golgi cisternae were specifically labeled. A and B antigens were demonstrated only in the glands of type A, B, and AB subjects, while H antigen was visualized in glands from individuals of all blood types. Moreover, differences were observed in the relative distribution of ABH antigens, depending on the type of gland.

ABO Blood-Group System

Type II regulatory subunit dimerization determines the subcellular localization of the cAMP-dependent protein kinase.

The type II cAMP-dependent protein kinase (PKA) is localized to specific subcellular environments through binding of dimeric regulatory subunits (RII) to anchoring proteins. Cytoskeletal localization occurs through RII dimer interaction with the PKA substrate molecule microtubule-associated protein 2 (MAP2). RII alpha deletion mutants and RII alpha/endonexin chimeras retained MAP2 binding activity if they contained the first 79 residues of the molecule. Disruption of RII alpha dimerization always prevented MAP2 interaction because 1) RII delta 1-14 (an amino-terminal deletion mutant lacking residues 1-14) was unable to bind MAP2 or form dimers, and 2) a modified RII alpha monomer including residues 1-14 did not bind MAP2. Chimeric proteins containing the first 30 residues of RII alpha fused to endonexin II formed dimers but did not bind MAP2. This suggested other side-chains between residues 30-79 also participate in MAP2 interaction. Peptide studies indicate additional contact with MAP2 may occur through an acidic region (residues 68-82) close to the RII autoinhibitor domain. Therefore, anchored PKA holoenzyme topology may position the catalytic subunit and MAP2 as to allow its preferential phosphorylation upon kinase activation.

Amino Acid Sequence