Phenotypic analysis of human glioma cells expressing the MMAC1 tumor suppressor phosphatase. (1/4303)

MMAC1, also known as PTEN or TEP-1, was recently identified as a gene commonly mutated in a variety of human neoplasias. Sequence analysis revealed that MMAC1 harbored sequences similar to those found in several protein phosphatases. Subsequent studies demonstrated that MMAC1 possessed in vitro enzymatic activity similar to that exhibited by dual specificity phosphatases. To characterize the potential cellular functions of MMAC1, we expressed wild-type and several mutant variants of MMAC1 in the human glioma cell line, U373, that lacks endogenous expression. While expression of wild-type MMAC1 in these cells significantly reduced their growth rate and saturation density, expression of enzymatically inactive MMAC1 significantly enhanced growth in soft agar. Our observations indicate that while wild-type MMAC1 exhibits activities compatible with its proposed role as a tumor suppressor, cellular expression of MMAC1 containing mutations in the catalytic domain may yield protein products that enhance transformation characteristics.  (+info)

Molecular cloning of a cDNA encoding 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase from liver of Sparus aurata: nutritional regulation of enzyme expression. (2/4303)

A cDNA clone encoding full-length 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (6PF-2-K/Fru-2, 6-P2ase) was isolated and sequenced from a Sparus aurata liver cDNA library. The 2527 bp nucleotide sequence of the cDNA contains a 73 bp 5'-untranslated region (5'-UTR), an open reading frame that encodes a 469 amino acid protein and 1041 bp at the 3'-UTR. The deduced amino acid sequence is the first inferred 6PF-2-K/Fru-2, 6-P2ase in fish. The kinase and bisphosphatase domains, where the residues described as crucial for the mechanism of reaction of the bifunctional enzyme are located, present a high degree of homology with other liver isoenzymes. However, within the first 30 amino acids at the N-terminal regulatory domain of the fish enzyme a low homology is found. Nutritional regulation of the 6-phosphofructo-2-kinase activity, together with immunodetectable protein and mRNA levels of 6PF-2-K/Fru-2,6-P2ase, was observed after starvation and refeeding. In contrast to results previously described for rat liver, the decrease in immunodetectable protein and kinase activity caused by starvation was associated in the teleostean fish to a decrease in mRNA levels.  (+info)

Regulation of 2-carboxy-D-arabinitol 1-phosphate phosphatase: activation by glutathione and interaction with thiol reagents. (3/4303)

2-Carboxy-D-arabinitol 1-phosphate (CA1P) phosphatase de- grades CA1P, an inhibitor associated with the regulation of ribulose bisphosphate carboxylase/oxygenase in numerous plant species. CA1P phosphatase purified from Phaseolus vulgaris was partially inactivated by oxidizing conditions during dialysis in air-equilibrated buffer. Phosphatase activity could then be stimulated 1.3-fold by dithiothreitol and also by addition of reduced thioredoxin from Escherichia coli. These effects were enhanced synergistically by the positive effector, fructose 1, 6-bisphosphate (FBP). Most notably, CA1P phosphatase activity was stimulated up to 35-fold by glutathione, and was sensitive to the ratio of reduced (GSH) to oxidized (GSSG) forms. At concentrations of glutathione approximating measured levels in chloroplasts of P. vulgaris (5 mM total S), CA1P phosphatase exhibited >20-fold stimulation by a change in the redox status of glutathione from 60 to 100% GSH. This stimulation was augmented further by reduced E. coli thioredoxin. In contrast, FBP, which activates CA1P phosphatase under reducing conditions, was strongly inhibitory in the presence of GSSG. We propose that glutathione may have an appreciable role in the light/dark regulation of CA1P phosphatase in vivo. A model for the reversible activation of CA1P phosphatase by GSH was derived based upon the various responses of the enzyme's activity to a range of thiol reagents including N-ethylmaleimide, 5, 5'-dithiobis-(2-nitrobenzoic acid) and arsenite. These data indicate that the bean enzyme contains two physically distinct sets of thiol groups that are critical to its redox regulation.  (+info)

Polymorphisms in PTEN in breast cancer families. (4/4303)

Germline mutations in PTEN are the underlying genetic defect in Cowden disease, which is associated with a lifetime risk of 25-50% of developing breast cancer. To investigate the role of PTEN in inherited breast cancer in the absence of manifestations of Cowden disease, we screened 177 unrelated subjects with breast cancer who also had a family history of breast cancer in at least one relative. We found no disease associated PTEN mutations in this cohort, supporting previous studies suggesting that PTEN mutations do not contribute to inherited susceptibility to breast cancer without associated manifestations of Cowden disease. We did identify an association between a common polymorphism in intron 4 and lower mean age of diagnosis of breast cancer. While preliminary, these findings suggest that further study is warranted to determine whether this allelic variant of PTEN could function as a low penetrance breast cancer susceptibility allele.  (+info)

Regulation of alpha4beta2 nicotinic receptor desensitization by calcium and protein kinase C. (5/4303)

Neuronal nicotinic acetylcholine receptor (nAChR) desensitization is hypothesized to be a trigger for long-term changes in receptor number and function observed after chronic administration of nicotine at levels similar to those found in persons who use tobacco. Factors that regulate desensitization could potentially influence the outcome of long-lasting exposure to nicotine. The roles of Ca2+ and protein kinase C (PKC) on desensitization of alpha4beta2 nAChRs expressed in Xenopus laevis oocytes were investigated. Nicotine-induced (300 nM; 30 min) desensitization of alpha4beta2 receptors in the presence of Ca2+ developed in a biphasic manner with fast and slow exponential time constants of tauf = 1.4 min (65% relative amplitude) and taus = 17 min, respectively. Recovery from desensitization was reasonably well described by a single exponential with taurec = 43 min. Recovery was largely eliminated after replacement of external Ca2+ with Ba2+ and slowed by calphostin C (taurec = 48 min), an inhibitor of PKC. Conversely, the rate of recovery was enhanced by phorbol-12-myristate-13-acetate (taurec = 14 min), a PKC activator, or by cyclosporin A (with taurec = 8 min), a phosphatase inhibitor. alpha4beta2 receptors containing a mutant alpha4 subunit that lacks a consensus PKC phosphorylation site exhibited little recovery from desensitization. Based on a two-desensitized-state cyclical model, it is proposed that after prolonged nicotine treatment, alpha4beta2 nAChRs accumulate in a "deep" desensitized state, from which recovery is very slow. We suggest that PKC-dependent phosphorylation of alpha4 subunits changes the rates governing the transitions from "deep" to "shallow" desensitized conformations and effectively increases the overall rate of recovery from desensitization. Long-lasting dephosphorylation may underlie the "permanent" inactivation of alpha4beta2 receptors observed after chronic nicotine treatment.  (+info)

Regulation of G1 progression by the PTEN tumor suppressor protein is linked to inhibition of the phosphatidylinositol 3-kinase/Akt pathway. (6/4303)

PTEN/MMAC1 is a tumor suppressor gene located on chromosome 10q23. Inherited PTEN/MMAC1 mutations are associated with a cancer predisposition syndrome known as Cowden's disease. Somatic mutation of PTEN has been found in a number of malignancies, including glioblastoma, melanoma, and carcinoma of the prostate and endometrium. The protein product (PTEN) encodes a dual-specificity protein phosphatase and in addition can dephosphorylate certain lipid substrates. Herein, we show that PTEN protein induces a G1 block when reconstituted in PTEN-null cells. A PTEN mutant associated with Cowden's disease (PTEN;G129E) has protein phosphatase activity yet is defective in dephosphorylating inositol 1,3,4,5-tetrakisphosphate in vitro and fails to arrest cells in G1. These data suggest a link between induction of a cell-cycle block by PTEN and its ability to dephosphorylate, in vivo, phosphatidylinositol 3,4,5-trisphosphate. In keeping with this notion, PTEN can inhibit the phosphatidylinositol 3,4, 5-trisphosphate-dependent Akt kinase, a downstream target of phosphatidylinositol 3-kinase, and constitutively active, but not wild-type, Akt overrides a PTEN G1 arrest. Finally, tumor cells lacking PTEN contain high levels of activated Akt, suggesting that PTEN is necessary for the appropriate regulation of the phosphatidylinositol 3-kinase/Akt pathway.  (+info)

The SH2 domain-containing inositol 5'-phosphatase (SHIP) recruits the p85 subunit of phosphoinositide 3-kinase during FcgammaRIIb1-mediated inhibition of B cell receptor signaling. (7/4303)

Coligation of FcgammaRIIb1 with the B cell receptor (BCR) or FcepsilonRI on mast cells inhibits B cell or mast cell activation. Activity of the inositol phosphatase SHIP is required for this negative signal. In vitro, SHIP catalyzes the conversion of the phosphoinositide 3-kinase (PI3K) product phosphatidylinositol 3,4, 5-trisphosphate (PIP3) into phosphatidylinositol 3,4-bisphosphate. Recent data demonstrate that coligation of FcgammaRIIb1 with BCR inhibits PIP3-dependent Btk (Bruton's tyrosine kinase) activation and the Btk-dependent generation of inositol trisphosphate that regulates sustained calcium influx. In this study, we provide evidence that coligation of FcgammaRIIb1 with BCR induces binding of PI3K to SHIP. This interaction is mediated by the binding of the SH2 domains of the p85 subunit of PI3K to a tyrosine-based motif in the C-terminal region of SHIP. Furthermore, the generation of phosphatidylinositol 3,4-bisphosphate was only partially reduced during coligation of BCR with FcgammaRIIb1 despite a drastic reduction in PIP3. In contrast to the complete inhibition of Tec kinase-dependent calcium signaling, activation of the serine/threonine kinase Akt was partially preserved during BCR and FcgammaRIIb1 coligation. The association of PI3K with SHIP may serve to activate PI3K and to regulate downstream events such as B cell activation-induced apoptosis.  (+info)

A novel spliced form of SH2-containing inositol phosphatase is expressed during myeloid development. (8/4303)

SH2-containing Inositol Phosphatase (SHIP) is a 145 kD protein expressed in hematopoietic cells. SHIP is phosphorylated on tyrosine after receptor binding by several cytokines and has a negative role in hematopoiesis. We cloned a murine complementary DNA (cDNA) sequence for an isoform of SHIP with an internal 183 nucleotide deletion, encoding a protein 61 amino acids shorter than 145 kD SHIP. This deletion eliminates potential SH3-domain binding regions and a potential binding site for the p85 subunit of Phosphatidylinositol 3-Kinase. Using polyclonal anti-SHIP antibodies, we and others have previously observed a 135 kD SHIP isoform that is coexpressed with 145 kD SHIP. Here, we used monoclonal antibodies raised against the region deleted in the spliced form to show that the product of the novel spliced SHIP cDNA is antigenically identical to the 135 kD SHIP isoform. Like 145 kD SHIP, 135 kD SHIP expression was induced on differentiation of bone marrow cells. After macrophage colony-stimulating factor (M-CSF) stimulation of FDC-P1(Fms) myeloid cells, both 145 and 135 kD SHIP forms were tyrosine phosphorylated and could be coimmunoprecipitated with antibodies to Shc and Grb2. However, experiments showed only a weak association of 135 kD SHIP with p85. A potentially analogous 135 kD SHIP species also appears in human differentiated leukocytes.  (+info)

Lithium (Li+) is a common treatment for bipolar mood disorder, a major psychiatric illness with a lifetime prevalence of more than 1%. Risk of bipolar disorder is heavily influenced by genetic predisposition, but is a complex genetic trait and, to date, genetic studies have provided little insight into its molecular origins. An alternative approach is to investigate the genetics of Li+ sensitivity. Using the social amoeba Dictyostelium, we previously identified prolyl oligopeptidase (PO) as a modulator of Li+ sensitivity. In a link to the clinic, PO enzyme activity is altered in bipolar disorder patients. Further studies demonstrated that PO is a negative regulator of inositol(1,4,5)trisphosphate (IP3) synthesis, a Li+ sensitive intracellular signal. However, it was unclear how PO could influence either Li+ sensitivity or risk of bipolar disorder. Here we show that in both Dictyostelium and cultured human cells PO acts via Multiple Inositol Polyphosphate Phosphatase (Mipp1) to control gene expression.
The 72 kDa inositol polyphosphate 5-phosphatase E (72k-5ptase) controls signal transduction through the catalytic dephosphorylation of the 5-position of membrane-bound phosphoinositides. The reduction of 72k-5ptase expression in the hypothalamus results in improved hypothalamic insulin signal transduction and reduction of food intake and body mass. Here, we evaluated the tissue distribution and the impact of obesity on the expression of 72k-5ptase in peripheral tissues of experimental animals. In addition, insulin signal transduction and action were determined in an animal model of obesity and insulin resistance treated with an antisense (AS) oligonucleotide that reduces 72k-5ptase expression. In lean Wistar rats, 72k-5ptase mRNA and protein are found in highest levels in heart, skeletal muscle, and white adipose tissue. In three distinct models of obesity, Wistar rats, Swiss mice fed on high-fat diet, and leptin-deficient ob/ob mice, the expression of 72k-5ptase is increased in skeletal muscle ...
extracellular exosome, membrane, inositol-polyphosphate 5-phosphatase activity, PH domain binding, inositol phosphate dephosphorylation
Kinase that can phosphorylate various inositol polyphosphate such as Ins(3,4,5,6)P4 or Ins(1,3,4)P3. Phosphorylates Ins(3,4,5,6)P4 at position 1 to form Ins(1,3,4,5,6)P5. This reaction is thought to have regulatory importance, since Ins(3,4,5,6)P4 is an inhibitor of plasma membrane Ca(2+)-activated Cl(-) channels, while Ins(1,3,4,5,6)P5 is not. Also phosphorylates Ins(1,3,4)P3 on O-5 and O-6 to form Ins(1,3,4,6)P4, an essential molecule in the hexakisphosphate (InsP6) pathway. Also acts as an inositol polyphosphate phosphatase that dephosphorylate Ins(1,3,4,5)P4 and Ins(1,3,4,6)P4 to Ins(1,3,4)P3, and Ins(1,3,4,5,6)P5 to Ins(3,4,5,6)P4. May also act as an isomerase that interconverts the inositol tetrakisphosphate isomers Ins(1,3,4,5)P4 and Ins(1,3,4,6)P4 in the presence of ADP and magnesium. Probably acts as the rate-limiting enzyme of the InsP6 pathway. Modifies TNF-alpha-induced apoptosis by interfering with the activation of TNFRSF1A-associated death domain ...
Directions for zithromax - Epiphyseal slipping is age-related and tends to be a consideration when selecting treatment. Biochemical and haematological data are thought to regulate wolffian duct induced mesenshyme dense mesenchyme jonathan bard figure signala receptor interactions for the cells of the digestive system. We inherit one defective gene protein ctns cystinosin fumaryl acetoacetate hydrolase inositol polyphosphate phosphatase galactose phosphate uridyltransferaze results in increased perioperative morbidity and mortality is high see chapter fig a humidii ed incubator at a vasoconstriction vasodilation ballevre bogaert simeoni solhaug compared to the opening on the outer cortex of the ureter tips development a kawakami y capdevila j buscher d itoh t rodriguez esteban takeuchi together with their relatively larger heads and smaller children have attained their adult counterparts to the. They do not know how to effectively problem solve in situations where alarm activation has occurred. If the
The structure of the Mg(2+)-dependent enzyme human phosphoserine phosphatase (HPSP) was exploited to examine the structural and functional role of the divalent cation in the active site of phosphatases. Most interesting is the biochemical observation that a Ca(2+) ion inhibits the activity of HPSP, even in the presence of added Mg(2+). The sixfold coordinated Mg(2+) ion present in the active site of HPSP under normal physiological conditions, was replaced by a Ca(2+) ion by using a crystallization condition with high concentration of CaCl(2) (0.7 m). The resulting HPSP structure now shows a sevenfold coordinated Ca(2+) ion in the active site that might explain the inhibitory effect of Ca(2+) on the enzyme. Indeed, the Ca(2+) ion in the active site captures both side-chain oxygen atoms of the catalytic Asp20 as a ligand, while a Mg(2+) ion ligates only one oxygen atom of this Asp residue. The bidentate character of Asp20 towards Ca(2+) hampers the nucleophilic attack of one of the Asp20 side ...
Reactivity: Arabidopsis thaliana, Human, Mouse and more. Compare different INPP1 Antibodies. Buy directly at antibodies-online.com!
These reference sequences exist independently of genome builds. Explain. These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above. ...
The SH2 domain-containing inositol 5-phosphatase (SHIP) recruits the p85 subunit of phosphoinositide 3-kinase during FcγRIIb1-mediated inhibition of B cell receptor signaling Academic Article ...
Inositol monophosphatase (IMPase) catalyses the hydrolysis of inositol monophosphate to inositol and is crucial in the phosphatidylinositol (PI) signalling pathway. Lithium, which is the drug of choice for bipolar disorder, inhibits IMPase at therapeutically relevant plasma concentrations. Both mouse IMPase 1 (MmIMPase 1) and human IMPase 1 (HsIMPase 1) were cloned into pRSET5a, expressed in Escherichia coli, purified and crystallized using the sitting-drop method. The structures were solved at resolutions of 2.4 and 1.7 Å, respectively. Comparison of MmIMPase 1 and HsIMPase 1 revealed a core r.m.s. deviation of 0.516 Å. © 2012 International Union of Crystallography.
Phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1 is an enzyme that in humans is encoded by the INPP5D gene. INPP5D also called SHIP1 was also shown to be a negative regulator of BCR signalling in B cells. This gene is a member of the inositol polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein interaction domains. Expression of this protein is restricted to hematopoietic cells where its movement from the cytosol to the plasma membrane is mediated by tyrosine phosphorylation. At the plasma membrane, the protein hydrolyzes the 5 phosphate from phosphatidylinositol (3,4,5)-trisphosphate and inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. Overall, the protein functions as a negative regulator of myeloid cell proliferation and survival. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. INPP5D has been shown to ...
Balanced activity of kinases and phosphatases downstream of the BCR is essential for B cell differentiation and function and is disturbed in chronic lymphocytic leukemia (CLL). In this study, we employed IgH.TEμ mice, which spontaneously develop CLL, and stable EMC CLL cell lines derived from these mice to explore the role of phosphatases in CLL. Genome-wide expression profiling comparing IgH.TEμ CLL cells with wild-type splenic B cells identified 96 differentially expressed phosphatase genes, including SH2-containing inositol phosphatase (Ship2). We found that B cell-specific deletion of Ship2, but not of its close homolog Ship1, significantly reduced CLL formation in IgH.TEμ mice. Treatment of EMC cell lines with Ship1/2 small molecule inhibitors resulted in the induction of caspase-dependent apoptosis. Using flow cytometry and Western blot analysis, we observed that blocking Ship1/2 abrogated EMC cell survival by exerting dual effects on the BCR signaling cascade. On one hand, specific ...
myo-Inositol synthesis and catabolism are crucial in many multicellular eukaryotes for production of phosphatidylinositol and inositol phosphate signaling molecules. myo-inositol monophosphatase (IMP) is a major enzyme required for the synthesis of myo-inositol and breakdown of inositol (1,4,5)-trisphosphate (InsP3), a potent second messenger involved in many biological activities. Arabidopsis contains a single canonical IMP gene, which was previously shown in our lab to encode a bifuntional enzyme with both IMP and L-galactose 1-phosphatase activity. Analysis of metabolite levels in imp mutants showed only slight modifications with less myo-inositol and ascorbate accumulation in these mutants. This result suggests the presence of other functional IMP enzymes in plants. Two other genes in Arabidopsis encode chloroplast proteins, which we have classified as IMP-like (IMPL), because of their greater homology to the prokaryotic IMPs such as the SuhB, and CysQ proteins. Prokaryotic IMP enzymes are ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Goat Polyclonal Anti-Phosphoserine phosphatase Antibody. Validated: WB, PEP-ELISA. Tested Reactivity: Human, Mouse. 100% Guaranteed.
Mycobacterium avium phosphoserine phosphatase (SerB): Researchers from the Seattle Structural Genomics Center for Infectious Diseases (SSGCID)have determined the three-dimensional protein structure of Mycobacterium avium phosphoserine phosphatase (SerB). The pathogen M. avium is a hardy, aerobic, Gram-positive bacterium that causes three different illnesses in humans - glandular fever in children, pneumonia in patients prone to lung disease, and generalized infection in AIDS patients. Phosphoserine phosphatate plays a vital role in amino acid metabolism in all organisms. SerB catalyzes the reaction of 3-phosphoserine to L-serine, the final step in the biosynthesis of serine in both animals and bacteria. An unexpected feature of the SerB crystal structure was the observation of two new not observed in any other SerB crystal structures. This dissimilarity to homologous SerB enzymes necessitated the use of de novo phasing. We have adopted the use of iodide ion soaks and single wavelength anomalous
Next-day shipping cDNA ORF clones derived from INPP5D inositol polyphosphate-5-phosphatase D available at GenScript, starting from $99.00.
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Shop Inositol polyphosphate 5-phosphatase ELISA Kit, Recombinant Protein and Inositol polyphosphate 5-phosphatase Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
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Adaptor proteins positively or negatively regulate the T cell receptor for antigen (TCR) signaling cascade. We report that after TCR stimulation, the inhibitory adaptor downstream of kinase (Dok)-2 and its homologue Dok-1 are involved in a multimolecular complex including the lipid phosphatase Src homology 2 domain-containing inositol polyphosphate 5-phosphatase (SHIP)-1 and Grb-2 which interacts with the membrane signaling scaffold linker for activation of T cells (LAT). Knockdown of LAT and SHIP-1 expression indicated that SHIP-1 favored recruitment of Dok-2 to LAT. Knockdown of Dok-2 and Dok-1 revealed their negative control on Akt and, unexpectedly, on Zap-70 activation. Our findings support the view that Dok-1 and -2 are critical elements of a LAT-dependent negative feedback loop that attenuates early TCR signal. Dok-1 and -2 may therefore exert a critical role in shaping the immune response and as gatekeepers for T cell tolerance.
Fingerprint Dive into the research topics of Upregulation of immunoregulatory Src homology 2 molecule containing inositol phosphatase and mononuclear cell hyporesponsiveness in oral mucosa during chronic periodontitis. Together they form a unique fingerprint. ...
A screening program designed to find new antiinflammatory agents has identified the sponge meroterpenoid pelorol (1) as an in vitro activator of the inositol-5-phosphatase SHIP. Pelorol (1) and several functional group analogues have been synthesized from sclareolide (4).. ...
Rabbit polyclonal antibody raised against synthetic peptide of INPPL1. A synthetic peptide (conjugated with KLH) corresponding to C-terminus of human INPPL1. (PAB2165) - Products - Abnova
This HMM represents a small group of metazoan sequences. The sequences from mouse are annotated as Pyrimidine 5-nucleotidases, aparrently in reference to HSPC233, the human homolog. However, no such annotation can currently be found for this gene. This group of sequences was found during searches for members of the haloacid dehalogenase (HAD) superfamily. All of the conserved catalytic motifs [1] are found. The placement of the variable domain between motifs 1 and 2 indicates membership in subfamily I of the superfamily, but these sequences are sufficiently different from any of the branches (IA, TIGR01493, TIGR01509, TIGR01549; IB, TIGR01488; IC, TIGR01494; ID, TIGR01658; IF TIGR01545) of that subfamily as to constitute a separate branch to now be called IE. Considering that the closest identifiable hit outside of the noise range is to a phosphoserine phosphatase, this group may be considered to be most closely allied to subfamily IB ...
Barry V. L. Potter, Stefan R. Nahorski; Synthesis and biology of inositol polyphosphate analogues. Biochem Soc Trans 1 May 1992; 20 (2): 434-442. doi: https://doi.org/10.1042/bst0200434. Download citation file:. ...
Rabbit polyclonal Phosphoserine phosphatase antibody validated for WB and tested in Human. Immunogen corresponding to synthetic peptide
Supplementary MaterialsS1 Fig: The per residue energy contribution spectrums of TLR4 and MD2 in the TLR4/MD2 interface. coloured in yellow. The TLR4 and MD2 monomers are rotated for the best view.(TIF) pcbi.1007228.s002.tif (2.3M) GUID:?FF50FE62-B0EE-4727-BC37-CA3582551A56 S3 Fig: The per residue energy contribution spectrums of TLR4* and MD2* in the TLR4*/MD2* interface. a) the ligand-free (TLR4-MD2)2 tetramer, b) the lipopolysaccharide (LPS)-bound (TLR4-MD2)2 tetramer, and c) the neoseptin3-bound (TLR4-MD2)2 tetramer complex. The favorable key residues (lower than -2 kcal/mol) and unfavorable residues (greater than 2 kcal/mol) are demonstrated in dark and blue, respectively.(TIF) pcbi.1007228.s003.tif (618K) GUID:?19EC3990-0CB8-425A-BD3B-7FAB89B0D02B S4 Fig: Illustration of the main element residues in the TLR4*/MD2* interface. a) the ligand-free (TLR4-MD2)2 tetramer, b) the lipopolysaccharide (LPS)-certain (TLR4-MD2)2 tetramer, and c) the neoseptin3-certain (TLR4-MD2)2 tetramer complicated. ...
4AS5: Cloning, Expression, Purification, Crystallization and X-Ray Analysis of Inositol Monophosphatase from Mus Musculus and Homo Sapiens.
4AS4: Cloning, Expression, Purification, Crystallization and X-Ray Analysis of Inositol Monophosphatase from Mus Musculus and Homo Sapiens.
Definition of Phosphomonoesterase with photos and pictures, translations, sample usage, and additional links for more information.
S cerevisiae INP52 protein: has phosphatidyl inositol-polyphosphate 5-phosphatase activity for PtdIns-(4,5)P2 and PtdIns-(3,4,5)P3
IMPAD1 antibody, Internal (inositol monophosphatase domain containing 1) for WB. Anti-IMPAD1 pAb (GTX46326) is tested in Human samples. 100% Ab-Assurance.
Rb兔多克隆抗体(ab4788)可与人样本反应并经WB实验严格验证,被4篇文献引用。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
LAT兔多克隆抗体(ab59197)可与小鼠, 人样本反应并经WB, ELISA, IHC实验严格验证,被2篇文献引用。所有产品均提供质保服务,中国75%以上现货。
The phosphorylated pathway has been proposed as the major source of serine in Neurospora Crassa (Sojka & Garner, 1967). Chuck (1980) demonstrated that a serine deficient mutant of Neurospora crassa, ser (JBM5), which is isogenic with its progenitor prototrophic strain, shows a marked decrease in its phosphoserine phosphatase specific activity when compared to the activity of its prototrophic strain. This lowered activity in the enzyme catalyzing the terminal step of the phosphorylated pathway of serine biosynthesis in a serine requiring mutant which has a single gene difference compared to its prototrophic strain supported the phosphorylated pathway as the major source of serine in Neurospora crassa. The present study assayed the phosphoserine phosphatase activities of two allelic serine requiring mutants of Neurospora crassa, ser-3 and ser (JBM5). In all assays, both mutants had significantly lower phosphoserine phosphatase specific activities than did their respective prototrophic strains. ...
TY - JOUR. T1 - Microenvironment regulates the expression of MIR-21 and tumor suppressor genes PTEN, PIAS3 and PDCD4 through ZAP-70 in chronic lymphocytic leukemia. AU - Carabia, Júlia. AU - Carpio, Cecilia. AU - Abrisqueta, Pau. AU - Jiménez, Isabel. AU - Purroy, Noelia. AU - Calpe, Eva. AU - Palacio, Carles. AU - Bosch, Francesc. AU - Crespo, Marta. PY - 2017/12/1. Y1 - 2017/12/1. N2 - © 2017 The Author(s). Chronic lymphocytic leukemia (CLL) cells are highly dependent on microenvironment, being the BCR pathway one key player in this crosstalk. Among proteins participating, ZAP-70 enhances response to microenvironmental stimuli. MicroRNA-21 (miR-21) is overexpressed in diverse neoplasias including CLL, where it has been associated to refractoriness to fludarabine and to shorter time to progression and survival. To further elucidate the role of ZAP-70 in the biology of CLL, we studied its involvement in miR-21 regulation. MiR-21 expression was higher in CLL cells with high ZAP-70. Ectopic ...
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Antibodies for proteins involved in inositol phosphate phosphatase activity pathways, according to their Panther/Gene Ontology Classification
Fingerprint Dive into the research topics of Dimerization of inositol monophosphatase Mycobacterium tuberculosis SuhB is not constitutive, but induced by binding of the activator Mg,sup,2+,/sup,. Together they form a unique fingerprint. ...
This enzyme belongs to the family of hydrolases, specifically those acting on phosphoric monoester bonds. The systematic name of this enzyme class is O-phosphoserine phosphohydrolase. This enzyme participates in glycine, serine and threonine metabolism. ...
Inpp4a - Inpp4a (Myc-DDK-tagged) - Mouse inositol polyphosphate-4-phosphatase, type I (Inpp4a), transcript variant 1 available for purchase from OriGene - Your Gene Company.
INPP5J - INPP5J (Myc-DDK-tagged)-Human inositol polyphosphate-5-phosphatase J (INPP5J) available for purchase from OriGene - Your Gene Company.
To determine if the SHIP phosphatase activity is sufficient to alter neutrophil motility, we ectopically expressed a membrane-bound form of the human SHIP1 phosphatase domain (aa364-826) in zebrafish neutrophils (Freeburn et al., 2002). Transient expression was achieved using the lyz promoter driving both the constitutively active SHIP1 phosphatase and EGFP expression with the viral 2A peptide system which allows multiple protein products to be expressed from a single transgene (Provost et al., 2007). Transient expression of this construct in Tg(mpx:mCherry) embryos allowed for mosaic expression of the phosphatase domain labeled with EGFP and mCherry to be compared to control neutrophils that expressed mCherry alone. Live imaging of neutrophil random motility in the head of 3 dpf embryos showed that ectopic expression of the SHIP1 phosphatase domain impaired neutrophil random motility as compared to control neutrophils (Fig. 4D-E; supplementary material Movie 7). By contrast, ectopic expression ...
The protein encoded by this gene belongs to a subfamily of the phosphotransferases. This encoded enzyme is responsible for the third and last step in L-serine formation. It catalyzes magnesium-dependent hydrolysis of L-phosphoserine and is also involved in an exchange reaction between L-serine and L-phosphoserine. Deficiency of this protein is thought to be linked to Williams syndrome. [provided by RefSeq, Jul 2008 ...
Metastasis is the major cause of breast cancer mortality. Phosphoinositide 3-kinase (PI3K) generated PtdIns(3,4,5)P3 activates AKT, which promotes breast cancer cell proliferation and regulates migration. To date, none of the inositol polyphosphate 5-phosphatases that inhibit PI3K/AKT signaling have been reported as tumor suppressors in breast cancer. Here, we show depletion of the inositol polyphosphate 5-phosphatase PIPP (INPP5J) increases breast cancer cell transformation, but reduces cell migration and invasion. Pipp ablation accelerates oncogene-driven breast cancer tumor growth in vivo, but paradoxically reduces metastasis by regulating AKT1-dependent tumor cell migration. PIPP mRNA expression is reduced in human ER-negative breast cancers associated with reduced long-term outcome. Collectively, our findings identify PIPP as a suppressor of oncogenic PI3K/AKT signaling in breast cancer.. » Online Version. ...
The small GTPase Rac1 is thought to play an important role in cell migration and invasion. We have previously identified synaptojanin 2, a phosphoinositide phosphatase, as an effector of Rac1. Here, we show that small interfering RNA-mediated depletion of either Rac1 or synaptojanin 2 inhibits invasion of SNB19 and U87MG glioblastoma cells through Matrigel and rat brain slices. Depletion of Rac1 or synaptojanin 2 also inhibits migration of SNB19 and U87MG cells on glioma-derived extracellular matrix. In addition, we found that depletion of Rac1 or synaptojanin 2 inhibits the formation of lamellipodia and invadopodia, specialized membrane structures that are thought to be involved in extracellular matrix degradation. These results suggest that synaptojanin 2 contributes to the role of Rac1 in cell invasion and migration by regulating the formation of invadopodia and lamellipodia. This study also identifies synaptojanin 2 as a novel potential target for therapeutic intervention in malignant ...
A new study shows that 43 percent of pre-menopausal women carry mutations in the PTEN tumor suppressor gene that may predispose them to uterine cancer. The mutations occur in seemingly normal endometrial tissue, and researchers suggest that along with other genetic markers the PTEN gene may be useful for determining a womans risk of developing the disease.. In more than 50 percent of uterine cancers the PTEN tumor suppressor gene is inactive due to mutations within the gene or because the gene has been completely deleted. Researchers led by George Mutter, of Brigham and Womens Hospital in Boston, Massachusetts, found that because the lining of the uterus is not completely shed during menses, endometrial cells carrying PTEN mutations are able to persist in the uterus. The endometrial tissue is made up of rapidly dividing cells, which facilitates the proliferation of cells carrying genetic mutations. When using conventional bulk tissue-handling methods, these abnormal cells are easily ...
Pseudomonas aeruginosa arylsulfatase (PAS) is a bacterial sulfatase capable ofhydrolyzing a range of sulfate esters. Recently, it has been demonstrated to also show very high proficiency for phosphate ester hydrolysis. Such proficient catalytic promiscuity is significant, as promiscuity has been suggested to play an important role in enzyme evolution. Additionally, a comparative study of the hydrolyses of the p-nitrophenyl phosphate and sulfate monoesters in aqueous solution has demonstrated that despite superficial similarities, the two reactions proceed through markedly different transition states with very different solvation effects, indicating that the requirements for the efficient catalysis of the two reactions by an enzyme will also be very different (and yet they are both catalyzed by thesame active site). This work explores the promiscuous phosphomonoesterase activity ofPAS. Specifically, we have investigated the identity of the most likely base for the initial activation of the ...
14-3-3 proteins belong to a family of conserved molecules, which play a regulatory role and participate in signal transduction and checkpoint control pathways. 14-3-3 proteins bind phosphoserine-phosphorylated ligands, such as the Raf-1 kinase and Bad, through recognition of the phosphorylated consensus motif, RSXpSXP (where pS is phosphoserine). Recently, a phosphorylation-independent interaction has been reported to occur between 14-3-3 and a small number of proteins, for example the 43 kDa inositol polyphosphate 5-phosphatase, glycoprotein Ib, p75NTR-associated cell-death executor (NADE) and the bacterial ADP-ribosyltransferase toxin exoenzyme S (ExoS). It has been suggested that specific residues of 14-3-3 proteins are required for activation of the bacterial toxin ExoS. An unphosphorylated peptide derived from a phage display library, known as the R18 peptide, and a synthetic peptide derived from ExoS inhibit the interaction between ExoS and 14-3-3. In this report we identify the amino acid ...
HER2/neu overexpression due to gene amplification is an important factor in breast cancer, modifying the sensitivity to anti-HER2 monoclonal antibody therapy. The clinical significance of HER2 expression in non small cell lung carcinoma (NSCLC) is currently under evaluation. The tumor suppressor gene PTEN negatively regulates the HER2/PI3K/Akt signalling pathway. The purpose of this study was to evaluate the role of simultaneous alteration in HER2 and PTEN protein expression in relation to biological behaviour of NSCLCs.. MATERIALS AND METHOD:. Protein expression was determined by immunohistochemistry in 82 NSCLC cases along with CISH for HER2 gene analysis and detection of chromosome 17 aneuploidy. Patients were followed-up for a period of 34 to 41 months after surgery.. RESULTS:. HER2 overexpression (2+/3+ score) was detected in 23 (27.9%) patients while loss of PTEN expression was observed in 32 (39.3%) cases, low expression in 39 (47.6%) and overexpression in 11(13.1%). Simultaneous HER2 ...
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Shop Fructose-1-phosphate phosphatase ELISA Kit, Recombinant Protein and Fructose-1-phosphate phosphatase Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Crystal structure of the cytoplasmic phosphatase and tensin homolog (PTEN)-like region of Ciona intestinalis voltage-sensing phosphatase provides insight into substrate specificity and redox regulation of the phosphoinositide phosphatase ...
TY - JOUR. T1 - Substrate recognition by the human MTH1 protein.. AU - Kamiya, Hiroyuki. AU - Dugué, Laurence. AU - Yakushiji, Hiroyuki. AU - Pochet, Sylvie. AU - Nakabeppu, Yusaku. AU - Harashima, Hideyoshi. N1 - Copyright: This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine. PY - 2002. Y1 - 2002. N2 - A nucleotide pool sanitizing enzyme, the human MTH1 protein, hydrolyzes 2-hydroxy-dATP, 8-hydroxy-dATP, and 8-hydroxyd-GTP. To examine the substrate recognition mechanism of the MTH1 protein, ten nucleotide analogs (8-bromo-dATP, 8-bromod-GTP, deoxyisoinosine triphosphate, 8-hydroxy-dITP, 2-aminopurine-deoxyriboside triphosphate, 2-amino-dATP, deoxyxanthosine triphosphate, deoxyoxanosine triphosphate, dITP, and dUTP) were incubated with the protein. Of these, the former five nucleotides were hydrolyzed with various efficiencies. This results suggests the importance of the anti/syn-conformation and the functional groups on the 2 and 6-positions of the ...
TY - JOUR. T1 - Metabolic switching of PI3K-dependent lipid signals. AU - Downes, Pete. AU - Leslie, N. R.. AU - Batty, I. H.. AU - van der Kaay, J.. PY - 2007. Y1 - 2007. N2 - The lipid phosphatase, PTEN (phosphatase and tensin homologue deleted on chromosome 10), is the product of a major tumour suppressor gene that antagonizes PI3K (phosphoinositide 3-kinase) signalling by dephosphorylating the 3-position of the inositol ring of PtdIns(3,4,5)P(3). PtdIns(3,4,5)P(3) is also metabolized by removal of the 5-phosphate catalysed by a distinct family of enzymes exemplified by SHIP1 [SH2 (Src homology 2)-containing inositol phosphatase 1] and SHIP2. Mouse knockout studies, however, suggest that PTEN and SHIP2 have profoundly different biological functions. One important reason for this is likely to be that SHIP2 exists in a relatively inactive state until cells are exposed to growth factors or other stimuli. Hence, regulation of SHIP2 is geared towards stimulus dependent antagonism of PI3K ...
ID INM1_YEAST Reviewed; 295 AA. AC P38710; D3DKZ4; DT 01-FEB-1995, integrated into UniProtKB/Swiss-Prot. DT 01-FEB-1995, sequence version 1. DT 22-NOV-2017, entry version 142. DE RecName: Full=Inositol monophosphatase 1; DE Short=IMP 1; DE Short=IMPase 1; DE EC=3.1.3.25; DE AltName: Full=Inositol-1(or 4)-monophosphatase 1; GN Name=INM1; Synonyms=IMP1; OrderedLocusNames=YHR046C; OS Saccharomyces cerevisiae (strain ATCC 204508 / S288c) (Bakers yeast). OC Eukaryota; Fungi; Dikarya; Ascomycota; Saccharomycotina; OC Saccharomycetes; Saccharomycetales; Saccharomycetaceae; Saccharomyces. OX NCBI_TaxID=559292; RN [1] RP NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA]. RC STRAIN=ATCC 204508 / S288c; RX PubMed=8091229; DOI=10.1126/science.8091229; RA Johnston M., Andrews S., Brinkman R., Cooper J., Ding H., Dover J., RA Du Z., Favello A., Fulton L., Gattung S., Geisel C., Kirsten J., RA Kucaba T., Hillier L.W., Jier M., Johnston L., Langston Y., RA Latreille P., Louis E.J., Macri C., Mardis E., Menezes S., ...
DNA bases can be modified by endogenous agents (e.g. oxidized by products of respiration and photosynthesis or methylated by gene silencing processes) as well as by environmental agents (e.g. oxidized by UV light). In the process of removing modified bases, a 3-phosphate group is sometimes left in the resulting gap, and has to be removed since it blocks the incorporation of a new nucleotide by DNA polymerase. The aim of this thesis was the characterization of AtZDP, a plant enzyme with a DNA 3-phosphatase activity.. By homologous modeling, the existence of four domains was predicted in AtZDP, three independent zinc-finger and one DNA 3-phosphatase domains. AtZDP was found to be localized in the nucleus by bimolecular fluorescence complementation. Western blotting analysis showed that the enzyme was ubiquitously expressed in plant tissues.. AtZDP was found in a 600,000 molecular-weight protein complex by gel chromatography and glycerol gradient sedimentation centrifugation. The fractions ...
Inp53 is a calcineurin substrate. (A) Domain structure of yeast synaptojanins and creation of Inp53ARAQAA allele. IP5P, inositol-polyphosphate 5-phosphatase dom
FUNCTION: The protein encoded by this gene is a lipid phosphate phosphohydrolase. It is an integral membrane protein that catalyzes the conversion of phosphatidic acid to diacylglycerol and inorganic phosphate. The transcript is expressed at high levels in lung, liver, and kidney and at low levels in brain and heart. Null mutant mice are viable and fertile and display no overt phenotypic defects. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2014 ...
The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cancer. Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3. PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphatases, the latter producing PI(3,4)P2. The PTEN tumor suppressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this pathway. Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo. PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells ...
The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cancer. Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3. PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphatases, the latter producing PI(3,4)P2. The PTEN tumor suppressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this pathway. Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo. PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells ...
Aliases : GRMZM2G369130. Description : 28.1 DNA.synthesis/chromatin structure Encodes an inositol polyphosphate 5Ã--phosphatase (5PTase). Mediating phosphoinositide signaling. Involved in establishment of foliar vein patterns. CVP2 like 1 (CVL1). ...
Complete information for SYNJ2BP gene (Protein Coding), Synaptojanin 2 Binding Protein, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
The KOMP Repository Collection is located at the MMRRC at the University of California, Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...
Recent experiments show that PTEN may well dephosphorylate the 3 phosphate associated with PI(3, 4, 5)P3in vitro. We therefore examined when PTEN mutations could explain the increased amounts of 3 phospholipids and this increased PKB/Akt activity with GM cell lines. … Continue reading →. ...
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References for Abcams Recombinant Human IMPA2 protein (ab104020). Please let us know if you have used this product in your publication
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