count source_label source_id relationship target_label target_id entity_type solr_id publication_id sentences 4 negative regulation of hydrolase activity GO:0051346 inhibits GO:0007586 Phenotype 6a64365e-2b48-11f0-b759-0050569a791b 10.1093/ajcn/78.3.610S The importance of slowing the rate of carbohydrate absorption has been illustrated recently by the results of the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) type 2 diabetes study, in which glucose-intolerant individuals had their risk of developing frank diabetes reduced by administration of acarbose, the α-glucosidase hydrolase inhibitor, which reduces the rate of carbohydrate digestion and absorption (92). 2 negative regulation of hydrolase activity GO:0051346 inhibits GO:0008283 Phenotype 52c2c2ac-bc37-11e5-8d2d-001a4ae51247 PMC2901331 The S-adenosylhomocysteine hydrolase inhibitor 3-Deazaneplanocin (DZNep) and the histone deacetylase inhibitor LBH589 (Panobinostat) reactivated the genes repressed by H3K27me3, depleted cells of the PRC2 component EZH2, reduced proliferation and increased apoptosis in human MM cell lines. 2 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype ddeb17f8-bc05-11e5-8abe-001a4ae51246 10.1016/j.yexcr.2006.10.003 Moreover, it was recently shown that apoptotic cell death caused by the AdoHcy hydrolase inhibitor, Adox, is largely dependent on the presence of the tumor suppressor p53, a sequence-specific transcription factor, to induce cell growth arrest or apoptosis[32]. 2 negative regulation of hydrolase activity GO:0051346 activates GO:0006915 Phenotype 52c2c2ac-bc37-11e5-8d2d-001a4ae51247 PMC2901331 The S-adenosylhomocysteine hydrolase inhibitor 3-Deazaneplanocin (DZNep) and the histone deacetylase inhibitor LBH589 (Panobinostat) reactivated the genes repressed by H3K27me3, depleted cells of the PRC2 component EZH2, reduced proliferation and increased apoptosis in human MM cell lines. 1 negative regulation of hydrolase activity GO:0051346 activates GO:0016571 Phenotype 18835662-bbe0-11e5-8abe-001a4ae51246 PMC3898630 More recently, a new study reported success in achieving reprogramming of mouse fibroblasts to iPSCs using only a cocktail of seven small molecules, including VPA, CHIR99021, 616452 (a TGFβ receptor inhibitor), parnate, forskolin (a cAMP pathway agonist), 3-deazaneplanocin A (an S-adenosylhomocysteine hydrolase inhibitor, blocking histone methylation), and TTNPB (an RAR agonist) (Hou et al., 2013). 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0016571 Phenotype 540555ac-f58e-11eb-959c-001a4a160176 30125527 The first identified SAH hydrolase inhibitor was 3-deazaneplanocin A (DZNep) (Glazer et al., 1986) that, when administered to cancer cell lines, is able to inhibit DNA and histone methylation (Miranda et al., 2009). 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0016571 Phenotype 6be64970-3534-11e8-a34b-001a4a160175 21719191 Indeed, 3-deazaneplanocin A (DZNep), an S-adenosylhomocysteine hydrolase inhibitor, was found to globally inhibit both repressive and active histone methylation marks as well as to induce apoptosis in cancer cells[170,171]. 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0009058 Phenotype f6994748-ca01-11e5-ab20-001a4ae51246 15640397 "The type I AdoHcy hydrolase inhibitor, MDL-28,842, inhibited the synthesis of TNF-α and was effective in the treatment of collagen-induced arthritis (Wolos et al., 1993c)." 1 negative regulation of hydrolase activity GO:0051346 activates GO:0008283 Phenotype a0e36fb2-ca02-11e5-be63-001a4ae51246 16326921 "Results DZ2002 Reduces OVA-Induced Lymphocyte Proliferation and Cytokine Production.Recently, we reported that the reversible AdoHcy hydrolase inhibitor DZ2002 had little effect on concanavalin A-stimulated T cells with regard to either proliferation or IL-2 production (Wu et al., 2005)." 1 negative regulation of hydrolase activity GO:0051346 activates GO:0007586 Phenotype b009705c-0800-11e8-bced-001a4a160176 PMC5758717 16 In the majority of cases, symptoms can be resolved with dietary management, particularly with a reduction of carbohydrate intake and supplementation of dietary fibers (bran, methycellulose) with meals.3Only 3–5% of patients require medical therapy such as octreotide, a somatostatin analog.3Another medical treatment is acarbose, an α-glycosidase hydrolase inhibitor that slows carbohydrate digestion in the small intestine. 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0030154 Phenotype 6edcb46e-351d-11e8-9192-001a4a160175 28579118 The methylation writer EZH2 is over-expressed in various cancers, including those of the thyroid (Sponziello et al., 2014; Borbone et al., 2011), and it can be targeted by the hydrolase inhibitor 3-deazaneplanocin A (DZNep) to induce differentiation and apoptosis in many types of cancer cells (Cui et al., 2014; Christofides et al., 2016). 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype a1d95726-bc4a-11e5-8d2d-001a4ae51247 10.1016/j.ejphar.2010.03.051 Recently, the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanocin A has been reported to induce apoptosis in breast cancer MCF-7 and colorectal HCT116 cells, through the depletion of polycomb repressor complex 2 components and inhibition of the histone methylation H3K27me3 (Tan et al., 2007). 1 negative regulation of hydrolase activity GO:0051346 activates GO:0006915 Phenotype 75ee2dbc-bc54-11e5-8abe-001a4ae51246 10.1016/j.biocel.2011.09.005 Epigenetic silencing of TXNIP by the polycomb repressive complex 2 (PRC2) It has been reported that a S-adenosylhomocysteine hydrolase inhibitor, 3-Deazaneplanocin A (DZNep) depletes EZH2 and the associated H3K27me3, and induces apoptosis in different cancer models (Tan et al., 2007). 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype f9980fe2-c484-11e5-9da3-001a4ae51247 22677129 DNZep, an S-adenosylhomocysteine hydrolase inhibitor, has been shown to eradicate tumor-initiating hepatocellular carcinoma cells and to induce apoptosis preferentially in cancer cells in other cancers, including AML.20-22DZNep inhibits S-adenosylhomocysteine hydrolase and causes the retention of S-adenosylhomocysteine, thereby inhibiting S-adenosyl-L-methionine–dependent methyltransferases such as EZH2.23However, DZNep is not a specific inhibitor of EZH2, so it affects other S-adenosyl-L-methionine–dependent methyltransferases as well. 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype 6edcb46e-351d-11e8-9192-001a4a160175 28579118 The methylation writer EZH2 is over-expressed in various cancers, including those of the thyroid (Sponziello et al., 2014; Borbone et al., 2011), and it can be targeted by the hydrolase inhibitor 3-deazaneplanocin A (DZNep) to induce differentiation and apoptosis in many types of cancer cells (Cui et al., 2014; Christofides et al., 2016). 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype 781906a8-bc21-11e5-9b9d-001a4ae51247 PMC3189508 We further noted that adenosine significantly increases protein tyrosine phosphatase (PTPase) activity in pulmonary vascular endothelial cells, and that PTPase inhibition attenuates apoptosis induced by adenosine, adenosine plus homocysteine (Ado/HC), and the SAH hydrolase inhibitor, MDL-28842. 1 negative regulation of hydrolase activity GO:0051346 activates GO:0006915 Phenotype 0f1edda4-bc2a-11e5-9b9d-001a4ae51247 PMC3914023 Among these inhibitors, 3-deazaneplanocin A (DZNep), aS-adenosylhomocysteine hydrolase inhibitor (Figure 7), depletes EZH2 and the associated H3K27me3 and can induce apoptosis in breast and colon cancer cells63. 1 negative regulation of hydrolase activity GO:0051346 activates GO:0006915 Phenotype 4733ea0e-c47c-11e5-91a7-001a4ae51247 22028491 "Our analysis focused on DZNep, an S-adenosylhomocysteine hydrolase inhibitor that has been shown to decrease DNA methylation, deplete PRC-2 components, and mediate cell-cycle arrest and apoptosis in cancer cells (21, 22)." 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype 6be64970-3534-11e8-a34b-001a4a160175 21719191 Indeed, 3-deazaneplanocin A (DZNep), an S-adenosylhomocysteine hydrolase inhibitor, was found to globally inhibit both repressive and active histone methylation marks as well as to induce apoptosis in cancer cells[170,171]. 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0006915 Phenotype 72a7a742-c8c0-11ee-b346-0050569a791b 10.1016/j.biopha.2023.114313 The RNAi-based therapeutics were considered as potential factors in targeting EZH2 signaling, until the development of DZNep, a potent SAH hydrolase inhibitor that mediates cancer apoptosis, was able to decrease H3K27me3 and suppressed PRC2 components[99,100]. 1 negative regulation of hydrolase activity GO:0051346 activates GO:0006306 Phenotype 4733ea0e-c47c-11e5-91a7-001a4ae51247 22028491 "Our analysis focused on DZNep, an S-adenosylhomocysteine hydrolase inhibitor that has been shown to decrease DNA methylation, deplete PRC-2 components, and mediate cell-cycle arrest and apoptosis in cancer cells (21, 22)." 1 negative regulation of hydrolase activity GO:0051346 activates GO:0032623 Phenotype a0e36fb2-ca02-11e5-be63-001a4ae51246 16326921 "Results DZ2002 Reduces OVA-Induced Lymphocyte Proliferation and Cytokine Production.Recently, we reported that the reversible AdoHcy hydrolase inhibitor DZ2002 had little effect on concanavalin A-stimulated T cells with regard to either proliferation or IL-2 production (Wu et al., 2005)." 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0042098 Phenotype 56372e18-cb8d-11e5-a7a8-001a4ae51246 11123369 The T-cell proliferation study measured by [3H]thymidine incorporation demonstrated that AdoHcy hydrolase inhibitor DHCaA (Ki= 90 nM) strongly inhibited T-cell proliferation with an IC50of 0.3 μM, which was much stronger than the IC50of 8 μM by DHCeA (Ki= 0.6 μM), a weaker inhibitor of AdoHcy hydrolase. 1 negative regulation of hydrolase activity GO:0051346 inhibits GO:0031099 Phenotype d204204e-bc3f-11e5-8d2d-001a4ae51247 PMC2845275 No Rme-specific immunoprecipitation was observed in the presence of adenosine dialdehyde (AdOx, a homocysteine hydrolase inhibitor that blocks the regeneration of the cellular methyl donorS-adenosyl methionine) (Bartel and Borchardt, 1984;Chenet al, 2004). 1 negative regulation of hydrolase activity GO:0051346 activates GO:0036269 Phenotype 5670134c-c8e8-11e5-9cb8-001a4ae51247 PMC2104793 Likewise, the fatty-acid amide hydrolase inhibitor, URB597 (0.1 and 0.3mgkg−1), decreased immobility – presumably by increasing swimming behavior – in the rat FST and also increased struggling behavior in the mouse TST[85]. 1 MESH:D010664 inhibits negative regulation of hydrolase activity GO:0051346 Phenotype 4aaed634-bbfe-11e5-9b9d-001a4ae51247 PMC3587710 Our biochemical assays demonstrated that SABP2 is able to hydrolyze 4-nitrophenyl butyrate, and its enzymatic activity can be entirely blocked by PMSF, a commonly used hydrolase inhibitor (Figure 1E).