PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 2468708-8 1989 When a mixture of highly purified T-PBL and autologous paraformaldehyde fixed accessory cells (AC) was cultivated, anti-H19 or anti-LFA-3 mAb bound to AC blocked T cell proliferation. paraform 55-71 H19 imprinted maternally expressed transcript Homo sapiens 120-123 33953304-4 2021 This study investigated the acute effect of CS/CSE on calcium homeostasis, a key regulator of ASM physiology and pathophysiology. Calcium 54-61 H19 imprinted maternally expressed transcript Homo sapiens 94-97 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Paclitaxel 0-10 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Doxorubicin 12-23 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Tamoxifen 25-34 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Erlotinib Hydrochloride 36-45 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Gefitinib 47-56 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Temozolomide 58-70 H19 imprinted maternally expressed transcript Homo sapiens 168-171 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Methotrexate 76-88 H19 imprinted maternally expressed transcript Homo sapiens 168-171 34038042-0 2021 Ginsenoside Rg3 suppresses ovarian cancer cell proliferation and invasion by inhibiting the expression of lncRNA H19. ginsenoside Rg3 0-15 H19 imprinted maternally expressed transcript Homo sapiens 113-116 34038042-12 2021 In terms of the mechanism, knockdown of H19 inhibited cell proliferation, migration and invasion, while overexpression of H19 reversed the inhibitory effect of Rg3 on the OC cells. ginsenoside Rg3 160-163 H19 imprinted maternally expressed transcript Homo sapiens 122-125 34038042-13 2021 In conclusion, ginsenoside Rg3 suppresses the proliferation, migration and invasion of OC cells by partially inhibiting the expression of lncRNA H19. ginsenoside Rg3 15-30 H19 imprinted maternally expressed transcript Homo sapiens 145-148 1090930-4 1975 The parent strain (asm-1), missing only glutamate synthase activity, also actively excretes NH4+ during early phases of its growth but eventually reutilizes the NN4+. Ammonium Compounds 92-96 H19 imprinted maternally expressed transcript Homo sapiens 19-24 1090930-4 1975 The parent strain (asm-1), missing only glutamate synthase activity, also actively excretes NH4+ during early phases of its growth but eventually reutilizes the NN4+. nn4+ 161-165 H19 imprinted maternally expressed transcript Homo sapiens 19-24 1090930-5 1975 A miximum yield of 4.0 mumol of NH4+/ml per 24 hr has been noted for asm-1 only during the growth period. Ammonia 32-35 H19 imprinted maternally expressed transcript Homo sapiens 69-74 33882812-16 2022 A novel crosstalk between miR-486-5p and H19 was observed highlighting a bi-directional relationship between them. mir-486-5p 26-36 H19 imprinted maternally expressed transcript Homo sapiens 41-44 32427885-8 2021 When participants were stratified based on baPWV cut-off values (< 1800 cm/s, 1800 to 1999 cm/s, >= 2000 cm/s), ASM index and HGS progressively decreased with an increase in baPWV levels (P for trend < 0.001). bapwv 174-179 H19 imprinted maternally expressed transcript Homo sapiens 112-115 32427885-9 2021 In multiple regression analysis, baPWV was significantly associated with ASM index (beta = -0.270, P < 0.001) and HGS (beta = -0.102, P < 0.001) independent of potential confounding factors. bapwv 33-38 H19 imprinted maternally expressed transcript Homo sapiens 73-76 33882812-17 2022 Hesperetin restored the expression of miR-486-5p, inhibited H19 lncRNA and ICAM-1 expression and selectively regressed mBC cell aggressiveness. hesperetin 0-10 H19 imprinted maternally expressed transcript Homo sapiens 60-63 33882812-18 2022 CONCLUSION: miR-486-5p and H19 are inter-connected upstream regulators for ICAM-1 building up miR-486-5p/H19/ICAM-1 axis that has been successfully tuned in mBC cells by hesperitin. hesperetin 170-180 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32813021-13 2021 HOXD-AS2 or H19 upregulation strongly promoted temozolomide resistance and MGMT expression. Temozolomide 47-59 H19 imprinted maternally expressed transcript Homo sapiens 12-15 33756038-9 2021 H19 knockdown suppressed glucose consumption, lactate production, and proliferation of GC cells via regulating the miR-519d-3p/LDHA axis. Lactic Acid 46-53 H19 imprinted maternally expressed transcript Homo sapiens 0-3 33756038-10 2021 Both miR-519d-3p depletion and LDHA overexpression could reverse the H19 knockdown-induced decrease in aerobic glycolysis and proliferation. mir-519d-3p 5-16 H19 imprinted maternally expressed transcript Homo sapiens 69-72 33912179-7 2021 Additionally, we show that expression of these CBZ-reactive TCRs in a reporter cell line, lacking endogenous alphabetaTCR, recapitulates the features of TCR activation reported for ASM-treated T cell lines/clones, providing a useful tool for further functional validations. Carbamazepine 47-50 H19 imprinted maternally expressed transcript Homo sapiens 181-184 34022752-7 2021 However, this difference was mainly driven by status epilepticus with in-hospital onset: among 108 patients, the time to first non-BZD ASM was longer during weekdays than during weekends/holidays (55.5 [28.8 to 103.5] minutes versus 28 [15.8 to 66.3] minutes, P = 0.003; adjusted HR = 1.65 [95% CI: 1.08 to 2.51], P = 0.01). N-BENZOYL-N'-BETA-D-GLUCOPYRANOSYL UREA 131-134 H19 imprinted maternally expressed transcript Homo sapiens 135-138 34022752-8 2021 CONCLUSIONS: The time to first non-BZD ASM in pediatric refractory status epilepticus is shorter on weekends/holidays than on weekdays, mainly driven by in-hospital onset status epilepticus. N-BENZOYL-N'-BETA-D-GLUCOPYRANOSYL UREA 35-38 H19 imprinted maternally expressed transcript Homo sapiens 39-42 33559139-7 2021 In fact, ACh also contributes to inflammation and remodeling of the airways and regulates the growth of ASM. Acetylcholine 9-12 H19 imprinted maternally expressed transcript Homo sapiens 104-107 33739984-18 2021 After adjusting for age, sex, obesity, HT, DM, DL, smoking, alcohol intake, and CRP, the risk of MetS decreased by 25% per 1Q increment in ASM% (P < 0.001). Alcohols 60-67 H19 imprinted maternally expressed transcript Homo sapiens 139-142 33635071-4 2021 Importantly, a remarkable PCE of 13.1% is obtained for TBD-S2:Y6 based ASM-OSCs, which is an attractive photovoltaic performance for ASM-OSCs. tert-butylserine 55-58 H19 imprinted maternally expressed transcript Homo sapiens 71-74 33635071-4 2021 Importantly, a remarkable PCE of 13.1% is obtained for TBD-S2:Y6 based ASM-OSCs, which is an attractive photovoltaic performance for ASM-OSCs. tert-butylserine 55-58 H19 imprinted maternally expressed transcript Homo sapiens 133-136 33314408-0 2021 H19/miR-107 / HMGB1 axis sensitizes laryngeal squamous cell carcinoma to cisplatin by suppressing autophagy in vitro and in vivo. Cisplatin 73-82 H19 imprinted maternally expressed transcript Homo sapiens 0-3 33669381-5 2021 Sulforaphane regulated the expression of all of five examined lncRNAs, but basal expression, biological function and inhibition of H19 were of highest significance. sulforaphane 0-12 H19 imprinted maternally expressed transcript Homo sapiens 131-134 33669381-10 2021 Together, we identified APOBEC3G as H19 target, and both are inhibited by sulforaphane in prevention of PDAC progression. sulforaphane 74-86 H19 imprinted maternally expressed transcript Homo sapiens 36-39 33146568-12 2021 The results of this study support our hypothesis that in hASM cells exposed to TNFalpha mitochondria are more fragmented, with an increase in mitochondrial biogenesis and mitochondrial volume density resulting in reduced O2 consumption rate per mitochondrion. Oxygen 221-223 H19 imprinted maternally expressed transcript Homo sapiens 57-61 33403385-9 2021 More interestingly, miR-193b-3p inhibitor could partially reverse the effect of H19 silencing. mir-193b 20-28 H19 imprinted maternally expressed transcript Homo sapiens 80-83 33505432-5 2020 The analysis of the correlation between OH-PAHs levels and methylation levels of imprinting genes showed that OH-PAHs are correlated with some CpG sites in H19, Peg3, and Meg3. oh-pahs 40-47 H19 imprinted maternally expressed transcript Homo sapiens 156-159 33505432-5 2020 The analysis of the correlation between OH-PAHs levels and methylation levels of imprinting genes showed that OH-PAHs are correlated with some CpG sites in H19, Peg3, and Meg3. oh-pahs 110-117 H19 imprinted maternally expressed transcript Homo sapiens 156-159 33058732-7 2021 Finally, an overexpression model of OPN1LW (a red light photoreceptor in the same opsin family) in human ASM cells showed an increase in intracellular cAMP levels following red light exposure compared to non-transfected cells (48+-13 vs. 13+-2.1 pmol cAMP/mg protein, p<0.01), suggesting a conserved photorelaxation mechanism for wavelengths of light that are more tissue penetrant. Cyclic AMP 151-155 H19 imprinted maternally expressed transcript Homo sapiens 105-108 33058732-7 2021 Finally, an overexpression model of OPN1LW (a red light photoreceptor in the same opsin family) in human ASM cells showed an increase in intracellular cAMP levels following red light exposure compared to non-transfected cells (48+-13 vs. 13+-2.1 pmol cAMP/mg protein, p<0.01), suggesting a conserved photorelaxation mechanism for wavelengths of light that are more tissue penetrant. Cyclic AMP 251-255 H19 imprinted maternally expressed transcript Homo sapiens 105-108 33058732-8 2021 Together, these results demonstrate that blue light photorelaxation in ASM is mediated by the OPN3 receptor interacting with Gs, which increases cAMP levels, activating PKA and modulated by GRK2. Cyclic AMP 145-149 H19 imprinted maternally expressed transcript Homo sapiens 71-74 33478972-4 2021 METHODS: Lentivirus-mediated overexpression, as well as antisense oligonucleotide-based silencing, modulated H19 in vitro. Oligonucleotides 66-81 H19 imprinted maternally expressed transcript Homo sapiens 109-112 33354655-6 2020 The ten identifiable metabolites included dicarboxylic fatty acids (five associated with LINE-1 or H19 methylation at q < 0.05) and 1-octadecanoyl-rac-glycerol (q < 0.0001 for association with H19 and q = 0.04 for association with LINE-1). dicarboxylic fatty acids 42-66 H19 imprinted maternally expressed transcript Homo sapiens 99-102 33179087-0 2021 Curcumin attenuates lncRNA H19-induced epithelial-mesenchymal transition in tamoxifen-resistant breast cancer cells. Curcumin 0-8 H19 imprinted maternally expressed transcript Homo sapiens 27-30 33179087-0 2021 Curcumin attenuates lncRNA H19-induced epithelial-mesenchymal transition in tamoxifen-resistant breast cancer cells. Tamoxifen 81-90 H19 imprinted maternally expressed transcript Homo sapiens 27-30 33179087-1 2021 The H19 long non-coding RNA is involved in the development of tamoxifen resistance in breast cancer. Tamoxifen 62-71 H19 imprinted maternally expressed transcript Homo sapiens 4-7 33179087-2 2021 However, the relationship between H19 and the metastatic potential and treatment options for tamoxifen-resistant (TAMR) breast cancer is not completely understood. Tamoxifen 93-102 H19 imprinted maternally expressed transcript Homo sapiens 34-37 33179087-4 2021 The present study aimed to investigate the role of H19 in MCF-7/TAMR cell epithelial-mesenchymal transition (EMT), migration and invasiveness, and to assess the ability of curcumin to inhibit H19-mediated effects. Curcumin 172-180 H19 imprinted maternally expressed transcript Homo sapiens 192-195 33179087-9 2021 In addition, following treatment with curcumin for 48 h, H19 expression was decreased in a dose-dependent manner. Curcumin 38-46 H19 imprinted maternally expressed transcript Homo sapiens 57-60 33179087-10 2021 Moreover, curcumin treatment for 48 h significantly attenuated H19-induced alterations in N-cadherin and E-cadherin expression levels. Curcumin 10-18 H19 imprinted maternally expressed transcript Homo sapiens 63-66 33179087-11 2021 Curcumin also prevented H19-induced invasion and migration. Curcumin 0-8 H19 imprinted maternally expressed transcript Homo sapiens 24-27 33179087-12 2021 The present study indicated that H19 may serve as a promoting factor of EMT, invasion and migration in MCF-7/TAMR cells, suggesting that curcumin may prevent H19-associated metastasis. Curcumin 137-145 H19 imprinted maternally expressed transcript Homo sapiens 33-36 33179087-12 2021 The present study indicated that H19 may serve as a promoting factor of EMT, invasion and migration in MCF-7/TAMR cells, suggesting that curcumin may prevent H19-associated metastasis. Curcumin 137-145 H19 imprinted maternally expressed transcript Homo sapiens 158-161 33396378-3 2020 Previous studies have shown that acute exposure to TNFalpha increases ASM force generation in response to muscarinic stimulation (hyper-reactivity) resulting in increased ATP consumption and increased tension cost. Adenosine Triphosphate 171-174 H19 imprinted maternally expressed transcript Homo sapiens 70-73 33162208-0 2021 LncRNA H19-mediated M2 polarization of macrophages promotes myofibroblast differentiation in pulmonary fibrosis induced by arsenic exposure. Arsenic 123-130 H19 imprinted maternally expressed transcript Homo sapiens 7-10 33162208-10 2021 The results indicated that H19 functioned as an miRNA sponge for let-7a, which was involved in arsenite-induced M2 polarization of macrophages and induced the myofibroblast differentiation phenotype by regulation of c-Myc. arsenite 95-103 H19 imprinted maternally expressed transcript Homo sapiens 27-30 33376397-7 2020 miR-138 can be used as the target gene of H19, and E2F2 can be negatively regulated by this miR, so miR-138 knockdown or E2F2 upregulation can weaken GCCs" biological behavior changes that were caused by H19 knockdown. mir-138 0-7 H19 imprinted maternally expressed transcript Homo sapiens 42-45 33376397-7 2020 miR-138 can be used as the target gene of H19, and E2F2 can be negatively regulated by this miR, so miR-138 knockdown or E2F2 upregulation can weaken GCCs" biological behavior changes that were caused by H19 knockdown. mir-138 0-7 H19 imprinted maternally expressed transcript Homo sapiens 204-207 33376397-7 2020 miR-138 can be used as the target gene of H19, and E2F2 can be negatively regulated by this miR, so miR-138 knockdown or E2F2 upregulation can weaken GCCs" biological behavior changes that were caused by H19 knockdown. mir-138 100-107 H19 imprinted maternally expressed transcript Homo sapiens 42-45 33376397-7 2020 miR-138 can be used as the target gene of H19, and E2F2 can be negatively regulated by this miR, so miR-138 knockdown or E2F2 upregulation can weaken GCCs" biological behavior changes that were caused by H19 knockdown. mir-138 100-107 H19 imprinted maternally expressed transcript Homo sapiens 204-207 33242392-4 2020 We demonstrate that fSHAPE patterns predict binding sites of known RBPs, such as iron response elements in both known loci and previously unknown loci in CDC34, SLC2A4RG, COASY, and H19. Iron 81-85 H19 imprinted maternally expressed transcript Homo sapiens 182-185 33510936-7 2021 Overexpression of H19 affected endothelial-mesenchymal transition in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas H19 knockdown reversed endothelial protective effects of icariin and reduced human umbilical vein endothelial cell migration. icariin 218-225 H19 imprinted maternally expressed transcript Homo sapiens 18-21 33270749-9 2020 VFA positively correlated with ASM and MetS, whereas ASM and MetS did not correlate with each other. Fatty Acids, Volatile 0-3 H19 imprinted maternally expressed transcript Homo sapiens 31-34 33270749-10 2020 Using VFA and ASM data in a MetS multiple linear regression model, the association between VFA and MetS remained positive, whereas a significant negative relationship emerged between ASM and MetS. Fatty Acids, Volatile 91-94 H19 imprinted maternally expressed transcript Homo sapiens 14-17 33510936-8 2021 Knockdown of H19 significantly downregulated oxidized low-density lipoprotein-induced E74-like factor 5 and upregulated miR-148b-3p, which was reversed by icariin. icariin 155-162 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32345117-8 2020 We observed that the H19 expression was significantly upregulated in chemotherapy-resistant breast cancer tissues and doxorubicin-resistant breast cancer cell lines. Doxorubicin 118-129 H19 imprinted maternally expressed transcript Homo sapiens 21-24 32345117-9 2020 Knockdown of H19 enhanced the sensitivity to doxorubicin both in vitro and in vivo. Doxorubicin 45-56 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32345117-0 2020 Long non-coding RNA H19 regulates proliferation and Doxorubicin resistance in MCF-7 cells by targeting PARP1. Doxorubicin 52-63 H19 imprinted maternally expressed transcript Homo sapiens 20-23 32345117-10 2020 While H19 overexpression developed doxorubicin-resistant in breast cancer cells both in vitro and in vivo. Doxorubicin 35-46 H19 imprinted maternally expressed transcript Homo sapiens 6-9 32345117-3 2020 The long noncoding RNA H19 (H19) is involved in various stages of tumorigenesis, however, its role in doxorubicin resistance remains unknown. Doxorubicin 102-113 H19 imprinted maternally expressed transcript Homo sapiens 23-26 32345117-3 2020 The long noncoding RNA H19 (H19) is involved in various stages of tumorigenesis, however, its role in doxorubicin resistance remains unknown. Doxorubicin 102-113 H19 imprinted maternally expressed transcript Homo sapiens 28-31 32345117-4 2020 The goal of this study was to evaluate the role of H19 in the development of doxorubicin-resistant breast cancer. Doxorubicin 77-88 H19 imprinted maternally expressed transcript Homo sapiens 51-54 32345117-6 2020 Both knockdown and overexpression of H19 were used to assess the sensitivity to doxorubicin in breast cancer cells in vitro and in vivo. Doxorubicin 80-91 H19 imprinted maternally expressed transcript Homo sapiens 37-40 32345117-7 2020 qRT-PCR and Western blot were used to explore the doxorubicin resistance mechanism of H19. Doxorubicin 50-61 H19 imprinted maternally expressed transcript Homo sapiens 86-89 32345117-11 2020 Furthermore, it was revealed that H19 negatively regulated PARP1 expression in breast cancer cells following doxorubicin treatment. Doxorubicin 109-120 H19 imprinted maternally expressed transcript Homo sapiens 34-37 32345117-12 2020 Knockdown of H19 sensitized breast cancer cells to doxorubicin by promoting PARP1 upregulation. Doxorubicin 51-62 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32345117-13 2020 H19 overexpression could recapitulate doxorubicin resistance by PARP1 downregulation. Doxorubicin 38-49 H19 imprinted maternally expressed transcript Homo sapiens 0-3 33058414-8 2020 During PL-induced chondrogenic differentiation of hUCMSCs, expression of H19 and SOX9 were increased, whereas miR-29b-3p expression was decreased. pl 7-9 H19 imprinted maternally expressed transcript Homo sapiens 73-76 32738709-0 2020 PFOS-induced placental cell growth inhibition is partially mediated by lncRNA H19 through interacting with miR-19a and miR-19b. perfluorooctane sulfonic acid 0-4 H19 imprinted maternally expressed transcript Homo sapiens 78-81 32738709-2 2020 The dysregulation of long non-coding RNA (lncRNA) H19 has been implicated in pregnancy complications such as intra-uterine growth retardation (IUGR), preeclampsia (PE), however, the expression and function of H19 in PFOS-exerted detrimental effects in the placenta remains to be unveiled. perfluorooctane sulfonic acid 216-220 H19 imprinted maternally expressed transcript Homo sapiens 50-53 32738709-2 2020 The dysregulation of long non-coding RNA (lncRNA) H19 has been implicated in pregnancy complications such as intra-uterine growth retardation (IUGR), preeclampsia (PE), however, the expression and function of H19 in PFOS-exerted detrimental effects in the placenta remains to be unveiled. perfluorooctane sulfonic acid 216-220 H19 imprinted maternally expressed transcript Homo sapiens 209-212 32738709-3 2020 Here, we explored the role of H19 in PFOS-induced placental toxicity. perfluorooctane sulfonic acid 37-41 H19 imprinted maternally expressed transcript Homo sapiens 30-33 32738709-8 2020 Furthermore, H19 appeared to partially improve the cell growth of HTR-8/SVneo cells exposed to PFOS via upregulation of miR-19a and miR-19b. perfluorooctane sulfonic acid 95-99 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32738709-9 2020 In summary, our findings revealed that H19/miR-19a and miR-19b/SMAD4 axis exerted important functions in PFOS-induced placenta cell toxicity. perfluorooctane sulfonic acid 105-109 H19 imprinted maternally expressed transcript Homo sapiens 39-42 33058414-9 2020 H19 overexpression promoted, whereas H19 silencing attenuated the PL-induced chondrogenic differentiation of hUCMSCs. pl 66-68 H19 imprinted maternally expressed transcript Homo sapiens 37-40 33058414-12 2020 In conclusion, PL induced chondrogenic differentiation of hUCMSCs by regulating the H19/miR-29b-3p/SOX9 axis. pl 15-17 H19 imprinted maternally expressed transcript Homo sapiens 84-87 33273918-6 2020 Catecholamines play a crucial role in regulating vascular smooth muscle (VSM), airway smooth muscle (ASM), and cardiac muscle (CM) function and tone. Catecholamines 0-14 H19 imprinted maternally expressed transcript Homo sapiens 101-104 32946927-5 2020 Mechanistically, H19 promoted ATG7 expression in pituitary tumor cells by inhibiting miR-93a expression. mir-93a 85-92 H19 imprinted maternally expressed transcript Homo sapiens 17-20 33273918-13 2020 In the ASM, beta 2-ARs are responsible for the bronchodilator effect, and T augments the expression of beta 2-ARs evoking an increase in the relaxing response to salbutamol. Albuterol 162-172 H19 imprinted maternally expressed transcript Homo sapiens 7-10 33097666-3 2020 Initial studies established multiple odorous molecules capable of increasing intracellular calcium ([Ca2+]i) in ASM cells, some of which were (paradoxically) associated with ASM relaxation. Calcium 91-98 H19 imprinted maternally expressed transcript Homo sapiens 112-115 33097666-4 2020 Subsequent studies showed a terpenoid molecule (nerol)-stimulated OR2W3 caused increases in [Ca2+]i and relaxation of ASM cells. Terpenes 28-37 H19 imprinted maternally expressed transcript Homo sapiens 118-121 33097666-8 2020 These findings demonstrate compartmentalization of Ca2+ signals dictates the odorant receptor OR2W3-induced ASM relaxation and identify a previously unrecognized E-C coupling mechanism that could be exploited in the development of therapeutics to treat obstructive lung diseases. Carbon 51-52 H19 imprinted maternally expressed transcript Homo sapiens 108-111 33097666-5 2020 Of note, OR2W3-evoked [Ca2+]i mobilization and ASM relaxation required Ca2+ flux through the store-operated calcium entry (SOCE) pathway and accompanied plasma membrane depolarization. Calcium 108-115 H19 imprinted maternally expressed transcript Homo sapiens 47-50 33097666-7 2020 Instead, ASM olfactory responses to the monoterpene nerol were predominated by the activity of Ca2+-activated chloride channels (TMEM16A), including the cystic fibrosis transmembrane conductance regulator (CFTR) expressed on endo(sarco)plasmic reticulum. Monoterpenes 40-51 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32996784-5 2020 In addition, ASM cells exposed to estrogen and testosterone for 24 h showed that testosterone significantly upregulates ACE2 expression in both males and females, whereas estrogen downregulates ACE2, albeit not significant compared with vehicle. Testosterone 47-59 H19 imprinted maternally expressed transcript Homo sapiens 13-16 33190991-7 2021 RESULTS: BCM yielded the following equation: ASM (kg) = -1.838 + 0.395 x total body water (L) + 0.105 x body weight (kg) + 1.231 x male sex - 0.026 x age (years) (R2 = 0.914, standard error of estimate = 1.35 kg). Water 84-89 H19 imprinted maternally expressed transcript Homo sapiens 45-48 33138822-6 2020 RESULTS: The expression of H19 mRNA was up-regulated in fibrotic lungs patients with IPF as well as in lungs tissues that obtained from bleomycin-treated mice. Bleomycin 136-145 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32996784-5 2020 In addition, ASM cells exposed to estrogen and testosterone for 24 h showed that testosterone significantly upregulates ACE2 expression in both males and females, whereas estrogen downregulates ACE2, albeit not significant compared with vehicle. Testosterone 81-93 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32916644-10 2020 Sodium valproate was the most frequently prescribed ASM in 2013, and its use decreased in girls in 2016. Valproic Acid 0-16 H19 imprinted maternally expressed transcript Homo sapiens 52-55 33035707-2 2020 Chromatin immunoprecipitation (ChIP)-sequencing analyses of human adipose-derived stem cells (hADSCs) showed that hypoxia induced trimethylation of 4th lysine residue of histone 3 (H3K4me3) in the H19 gene, among the 40 known human imprinted genes, to the greatest extent. Lysine 152-158 H19 imprinted maternally expressed transcript Homo sapiens 197-200 32916644-11 2020 Levetiracetam increased from 19.10 % in 2013 to 28.09 % in 2018 and became the most common ASM at the end of this study. Levetiracetam 0-13 H19 imprinted maternally expressed transcript Homo sapiens 91-94 32916644-15 2020 Levetiracetam has replaced sodium valproate as the most frequently prescribed ASM in pediatric patients. Levetiracetam 0-13 H19 imprinted maternally expressed transcript Homo sapiens 78-81 31994191-0 2020 Exosome-mediated transfer of long noncoding RNA H19 induces doxorubicin resistance in breast cancer. Doxorubicin 60-71 H19 imprinted maternally expressed transcript Homo sapiens 48-51 33106653-2 2020 We report that a long noncoding RNA (lncRNA), H19, associates with dystrophin and inhibits E3-ligase-dependent polyubiquitination at Lys 3584 (referred to as Ub-DMD) and its subsequent protein degradation. Lysine 133-136 H19 imprinted maternally expressed transcript Homo sapiens 46-49 33106653-5 2020 H19 RNA oligonucleotides conjugated with agrin (AGR-H19) and nifenazone competed with or inhibited TRIM63. Oligonucleotides 8-24 H19 imprinted maternally expressed transcript Homo sapiens 0-3 33106653-5 2020 H19 RNA oligonucleotides conjugated with agrin (AGR-H19) and nifenazone competed with or inhibited TRIM63. nifenazone 61-71 H19 imprinted maternally expressed transcript Homo sapiens 0-3 31994191-3 2020 In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. Doxorubicin 103-114 H19 imprinted maternally expressed transcript Homo sapiens 46-49 31994191-3 2020 In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. Doxorubicin 116-119 H19 imprinted maternally expressed transcript Homo sapiens 46-49 31994191-4 2020 As a result, increased H19 expression was observed in DOX-resistant breast cancer cells in comparison with the corresponding parental cells. Doxorubicin 54-57 H19 imprinted maternally expressed transcript Homo sapiens 23-26 31994191-5 2020 Suppression of H19 significantly lowered DOX resistance by decreasing cell viability, lowering colony-forming ability, and inducing apoptosis. Doxorubicin 41-44 H19 imprinted maternally expressed transcript Homo sapiens 15-18 31994191-8 2020 Taken together, H19 could be delivered by exosomes to sensitive cells, leading to the dissemination of DOX resistance. Doxorubicin 103-106 H19 imprinted maternally expressed transcript Homo sapiens 16-19 31994191-9 2020 Our finding highlights the potential of exosomal H19 as a molecular target to reduce DOX resistance. Doxorubicin 85-88 H19 imprinted maternally expressed transcript Homo sapiens 49-52 33101034-0 2020 Long Non-Coding RNA H19 Positively Associates With Aspirin Resistance in the Patients of Cerebral Ischemic Stroke. Aspirin 51-58 H19 imprinted maternally expressed transcript Homo sapiens 20-23 33061615-13 2020 MiR-491-5p inhibition abrogated the activities of proliferation, apoptosis, migration and invasion affected by H19 knockdown. CHEMBL3740941 8-10 H19 imprinted maternally expressed transcript Homo sapiens 111-114 33101034-9 2020 Results: Plasma H19 was significantly up-regulated in patients with aspirin resistance (p=0.0203), and the H19 levels were positively associated with urine 11dhTXB2/creatinine (R=0.04364, p=0.0106) and positively associated with the level of 8-iso-PGF2alpha (R=0.04561, p=0.0089). Aspirin 68-75 H19 imprinted maternally expressed transcript Homo sapiens 16-19 33101034-5 2020 Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance. Aspirin 135-142 H19 imprinted maternally expressed transcript Homo sapiens 117-120 33101034-9 2020 Results: Plasma H19 was significantly up-regulated in patients with aspirin resistance (p=0.0203), and the H19 levels were positively associated with urine 11dhTXB2/creatinine (R=0.04364, p=0.0106) and positively associated with the level of 8-iso-PGF2alpha (R=0.04561, p=0.0089). Creatinine 165-175 H19 imprinted maternally expressed transcript Homo sapiens 107-110 33040789-3 2020 To investigate the relationship between vincristine (VCR) resistance and Long noncoding RNA H19 (Lnc-RNA H19) in multiple myeloma (MM) this experiment was set up. Vincristine 40-51 H19 imprinted maternally expressed transcript Homo sapiens 92-95 33101034-5 2020 Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance. Aspirin 135-142 H19 imprinted maternally expressed transcript Homo sapiens 117-120 33101034-5 2020 Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance. Aspirin 135-142 H19 imprinted maternally expressed transcript Homo sapiens 117-120 33101034-9 2020 Results: Plasma H19 was significantly up-regulated in patients with aspirin resistance (p=0.0203), and the H19 levels were positively associated with urine 11dhTXB2/creatinine (R=0.04364, p=0.0106) and positively associated with the level of 8-iso-PGF2alpha (R=0.04561, p=0.0089). 8-epi-prostaglandin F2alpha 242-257 H19 imprinted maternally expressed transcript Homo sapiens 107-110 33101034-5 2020 Since the relationship between H19 and aspirin resistance have never been reported, herein, we aimed to evaluate the H19 expression in aspirin-resistant ischemic stroke patients and subsequently, ascertain the ability of H19 to diagnose aspirin resistance. Aspirin 135-142 H19 imprinted maternally expressed transcript Homo sapiens 117-120 33101034-10 2020 The ROC curves indicated that H19 can sensitively and specifically diagnose aspirin resistance (area under the curve, 0.8005; 95% CI, 0.7301-0.8710; p < 0.0001; specificity, 75.86207%; sensitivity, 73.84615%.). Aspirin 76-83 H19 imprinted maternally expressed transcript Homo sapiens 30-33 33101034-11 2020 H19 is an independent risk factor for aspirin resistance (OR=1.129, p=0.0321), and aspirin resistance and H19 are closely related with ischemic stroke recurrence. Aspirin 38-45 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32579217-6 2020 In vitro, hepatocyte injury triggered the increase of Sox9/H19 axis, whereas silence of H19 greatly alleviated the H2O2-induced hepatocyte apoptosis, suggesting that H19 functions as a downstream effector of Sox9 signaling and is involved in hepatocyte apoptosis. Hydrogen Peroxide 115-119 H19 imprinted maternally expressed transcript Homo sapiens 88-91 33101034-12 2020 Conclusions: H19 is closely associated with aspirin resistance, and H19 probably induces aspirin resistance through increasing the production of 8-iso-prostaglandin-2alpha. Aspirin 44-51 H19 imprinted maternally expressed transcript Homo sapiens 13-16 33101034-12 2020 Conclusions: H19 is closely associated with aspirin resistance, and H19 probably induces aspirin resistance through increasing the production of 8-iso-prostaglandin-2alpha. Aspirin 89-96 H19 imprinted maternally expressed transcript Homo sapiens 68-71 33101034-12 2020 Conclusions: H19 is closely associated with aspirin resistance, and H19 probably induces aspirin resistance through increasing the production of 8-iso-prostaglandin-2alpha. 8-iso-prostaglandin-2alpha 145-171 H19 imprinted maternally expressed transcript Homo sapiens 68-71 33101034-13 2020 Besides which, H19 may serve as a serological marker for diagnosing aspirin resistance with high specificity and sensitivity, and the test of H19 could give clues to the recurrence of ischemic stroke. Aspirin 68-75 H19 imprinted maternally expressed transcript Homo sapiens 15-18 33041794-10 2020 UCL 1684 reduced carbachol-evoked ASM contractions (>90%, IC50 0.43 muM), and calcium mobilization in rodent and human lung ASM cells. Carbachol 17-26 H19 imprinted maternally expressed transcript Homo sapiens 34-37 32420678-0 2020 Long noncoding RNA H19 acts as a miR-340-3p sponge to promote epithelial-mesenchymal transition by regulating YWHAZ expression in paclitaxel-resistant breast cancer cells. Paclitaxel 130-140 H19 imprinted maternally expressed transcript Homo sapiens 19-22 32420678-5 2020 In this study, it was detected that the expression level of H19 was increased in BC paclitaxel-resistant (PR) cells subline (MCF-7/PR) in comparison with MCF-7 parental cells. Paclitaxel 84-94 H19 imprinted maternally expressed transcript Homo sapiens 60-63 32579217-6 2020 In vitro, hepatocyte injury triggered the increase of Sox9/H19 axis, whereas silence of H19 greatly alleviated the H2O2-induced hepatocyte apoptosis, suggesting that H19 functions as a downstream effector of Sox9 signaling and is involved in hepatocyte apoptosis. Hydrogen Peroxide 115-119 H19 imprinted maternally expressed transcript Homo sapiens 88-91 32633936-2 2020 Here we design a series of superhydrophilic aromatic sulfonate materials (ASMs) comprising successively increasing conjugated systems and ionizable groups (ASM-1, ASM-2, ASM-3) to develop chlorine-resistant membrane via chemical modification. Chlorine 188-196 H19 imprinted maternally expressed transcript Homo sapiens 156-161 32921982-0 2020 Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway. Levonorgestrel 0-14 H19 imprinted maternally expressed transcript Homo sapiens 50-53 32921982-1 2020 Purpose: To explore the mechanism of levonorgestrel (LNG)-ameliorating adenomyosis through long non-coding RNA H19 (lncRNA H19)/miR-17/Toll-like receptor 4 (TLR4) pathway. Levonorgestrel 37-51 H19 imprinted maternally expressed transcript Homo sapiens 111-114 32921982-1 2020 Purpose: To explore the mechanism of levonorgestrel (LNG)-ameliorating adenomyosis through long non-coding RNA H19 (lncRNA H19)/miR-17/Toll-like receptor 4 (TLR4) pathway. Levonorgestrel 37-51 H19 imprinted maternally expressed transcript Homo sapiens 123-126 32439420-0 2020 LncRNA H19 downregulation confers erlotinib resistance through upregulation of PKM2 and phosphorylation of AKT in EGFR-mutant lung cancers. Erlotinib Hydrochloride 34-43 H19 imprinted maternally expressed transcript Homo sapiens 7-10 32439420-5 2020 H19 downregulation contributed to erlotinib resistance through interaction and upregulation of PKM2, which enhanced the phosphorylation of AKT. Erlotinib Hydrochloride 34-43 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32439420-8 2020 These findings revealed a novel mechanism of low-level H19 in the regulation of erlotinib resistance in EGFR-mutant lung cancers. Erlotinib Hydrochloride 80-89 H19 imprinted maternally expressed transcript Homo sapiens 55-58 32889156-4 2020 METHODS: An assay for measuring cyclic adenosine monophosphate (cAMP) in ASM derived from healthy donors was adapted to provide a biochemical surrogate for ASM relaxation. Adenosine 39-48 H19 imprinted maternally expressed transcript Homo sapiens 73-76 32485786-0 2020 Galangin promotes cell apoptosis through suppression of H19 expression in hepatocellular carcinoma cells. galangin 0-8 H19 imprinted maternally expressed transcript Homo sapiens 56-59 32485786-4 2020 Furthermore, H19 expression pattern was also determined in MHCC97H cells following treatment with galangin. galangin 98-106 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32485786-9 2020 Besides, the expression of H19 was markedly reduced following treatment with galangin in MHCC97H cells. galangin 77-85 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32485786-15 2020 These results indicated that galangin promoted cell apoptosis through reduced the expression of H19 and miR675 in MHCC97H cells. galangin 29-37 H19 imprinted maternally expressed transcript Homo sapiens 96-99 32485786-17 2020 CONCLUSION: Our data suggested that galangin has a crucial role in hepatocarcinogenesis through regulating the expression pattern of H19. galangin 36-44 H19 imprinted maternally expressed transcript Homo sapiens 133-136 32812390-5 2020 As an alternative, we hypothesized that cytoskeletal remodeling within ASM cells results in increased internal loading of contractile proteins that slows cross-bridge cycling and ATP hydrolysis rates. Adenosine Triphosphate 179-182 H19 imprinted maternally expressed transcript Homo sapiens 71-74 32812390-6 2020 To test this hypothesis, we simultaneously measured isometric force and ATP hydrolysis rate in permeabilized porcine ASM strips activated by Ca2+ (pCa 4.0). Adenosine Triphosphate 72-75 H19 imprinted maternally expressed transcript Homo sapiens 117-120 32889156-4 2020 METHODS: An assay for measuring cyclic adenosine monophosphate (cAMP) in ASM derived from healthy donors was adapted to provide a biochemical surrogate for ASM relaxation. Cyclic AMP 64-68 H19 imprinted maternally expressed transcript Homo sapiens 73-76 32889156-5 2020 Concentration-response curves for cAMP were established for three drugs that elicit ASM relaxation: isoprenaline (ISO), forskolin (FOR) and salbutamol sulphate. Cyclic AMP 34-38 H19 imprinted maternally expressed transcript Homo sapiens 84-87 32889156-5 2020 Concentration-response curves for cAMP were established for three drugs that elicit ASM relaxation: isoprenaline (ISO), forskolin (FOR) and salbutamol sulphate. Isoproterenol 100-112 H19 imprinted maternally expressed transcript Homo sapiens 84-87 32889156-5 2020 Concentration-response curves for cAMP were established for three drugs that elicit ASM relaxation: isoprenaline (ISO), forskolin (FOR) and salbutamol sulphate. Isoproterenol 114-117 H19 imprinted maternally expressed transcript Homo sapiens 84-87 32889156-5 2020 Concentration-response curves for cAMP were established for three drugs that elicit ASM relaxation: isoprenaline (ISO), forskolin (FOR) and salbutamol sulphate. Albuterol 140-159 H19 imprinted maternally expressed transcript Homo sapiens 84-87 32889156-8 2020 RESULTS: ASM responded with concentration dependent increases in cAMP when exposed to 10-9 to 10-5 M (ISO), (FOR) or salbutamol sulphate solutions for 15 or 30 min. Cyclic AMP 65-69 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32889156-8 2020 RESULTS: ASM responded with concentration dependent increases in cAMP when exposed to 10-9 to 10-5 M (ISO), (FOR) or salbutamol sulphate solutions for 15 or 30 min. Albuterol 117-136 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32889156-9 2020 Salbutamol formulated with different counter ions elicited differential cAMP responses in ASM (xinafoate>base=sulphate) suggesting that this bioassay could discriminate between formulations with different potency. Albuterol 0-10 H19 imprinted maternally expressed transcript Homo sapiens 90-93 32889156-9 2020 Salbutamol formulated with different counter ions elicited differential cAMP responses in ASM (xinafoate>base=sulphate) suggesting that this bioassay could discriminate between formulations with different potency. Cyclic AMP 72-76 H19 imprinted maternally expressed transcript Homo sapiens 90-93 32889156-9 2020 Salbutamol formulated with different counter ions elicited differential cAMP responses in ASM (xinafoate>base=sulphate) suggesting that this bioassay could discriminate between formulations with different potency. xinafoate 95-104 H19 imprinted maternally expressed transcript Homo sapiens 90-93 32889156-9 2020 Salbutamol formulated with different counter ions elicited differential cAMP responses in ASM (xinafoate>base=sulphate) suggesting that this bioassay could discriminate between formulations with different potency. Sulfates 110-118 H19 imprinted maternally expressed transcript Homo sapiens 90-93 32627034-0 2020 Long non-coding RNA H19 is involved in sorafenib resistance in hepatocellular carcinoma by upregulating miR-675. Sorafenib 39-48 H19 imprinted maternally expressed transcript Homo sapiens 20-23 32299856-2 2020 TRPV4 activation causes contraction of human ASM via the release of cysteinyl leukotrienes (cysLTs) but the mechanism is unknown. cysteinyl-leukotriene 68-90 H19 imprinted maternally expressed transcript Homo sapiens 45-48 32299856-2 2020 TRPV4 activation causes contraction of human ASM via the release of cysteinyl leukotrienes (cysLTs) but the mechanism is unknown. cysteinyl-leukotriene 92-98 H19 imprinted maternally expressed transcript Homo sapiens 45-48 32299856-7 2020 GSK1016790A increased [Ca2+]i and released ATP in human ASM cells without causing contraction. N-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamide 0-11 H19 imprinted maternally expressed transcript Homo sapiens 56-59 32299856-7 2020 GSK1016790A increased [Ca2+]i and released ATP in human ASM cells without causing contraction. Adenosine Triphosphate 43-46 H19 imprinted maternally expressed transcript Homo sapiens 56-59 32299856-11 2020 CONCLUSIONS: TRPV4 activation increases [Ca2+]i and releases ATP from ASM cells triggering P2X4-dependent release of cysLTs from mast cells resulting in ASM contraction. Adenosine Triphosphate 61-64 H19 imprinted maternally expressed transcript Homo sapiens 70-73 32299856-11 2020 CONCLUSIONS: TRPV4 activation increases [Ca2+]i and releases ATP from ASM cells triggering P2X4-dependent release of cysLTs from mast cells resulting in ASM contraction. Adenosine Triphosphate 61-64 H19 imprinted maternally expressed transcript Homo sapiens 153-156 32371379-7 2020 H19 relieved miR-1-3p-induced inhibition of CCL2 expression by acting as a ceRNA. mir-1-3p 13-21 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32356199-5 2020 miR-585-3p was verified to be a target of lncRNA H19 and was negatively regulated by H19. mir-585-3p 0-10 H19 imprinted maternally expressed transcript Homo sapiens 49-52 32356199-5 2020 miR-585-3p was verified to be a target of lncRNA H19 and was negatively regulated by H19. mir-585-3p 0-10 H19 imprinted maternally expressed transcript Homo sapiens 85-88 32356199-7 2020 In vitro results indicated that H19 inhibited the apoptosis of MPP+ treated neuroblastoma cells by regulating of miR-585-3p. mangion-purified polysaccharide (Candida albicans) 63-67 H19 imprinted maternally expressed transcript Homo sapiens 32-35 32356199-7 2020 In vitro results indicated that H19 inhibited the apoptosis of MPP+ treated neuroblastoma cells by regulating of miR-585-3p. mir-585-3p 113-123 H19 imprinted maternally expressed transcript Homo sapiens 32-35 32627034-5 2020 In the present study, CCK-8 assay, RT-qPCR, EdU staining, immunofluorescence staining, and western blot analysis were used to detect the effect of lncRNA H19 on sorafenib resistance of HCC cells. Sorafenib 161-170 H19 imprinted maternally expressed transcript Homo sapiens 154-157 32627034-6 2020 H19 expression was found to be negatively related to sorafenib sensitivity in HCC cells. Sorafenib 53-62 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32435188-3 2020 Using human airway smooth muscle (ASM) cells and murine precision-cut lung slices, we discovered that pitavastatin significantly inhibited basal-, histamine-, and methacholine (MCh)-induced ASM contraction. pitavastatin 102-114 H19 imprinted maternally expressed transcript Homo sapiens 34-37 32606925-0 2020 Exosomal Transfer of lncRNA H19 Promotes Erlotinib Resistance in Non-Small Cell Lung Cancer via miR-615-3p/ATG7 Axis. Erlotinib Hydrochloride 41-50 H19 imprinted maternally expressed transcript Homo sapiens 28-31 32606925-3 2020 This study aims to investigate the effect of exosomal lncRNA H19 on erlotinib resistance in NSCLC and the underlying mechanism. Erlotinib Hydrochloride 68-77 H19 imprinted maternally expressed transcript Homo sapiens 61-64 32606925-9 2020 Xenograft tumor models were used to investigate the effect of H19 on erlotinib resistance in vivo. Erlotinib Hydrochloride 69-78 H19 imprinted maternally expressed transcript Homo sapiens 62-65 32606925-11 2020 Results: H19 was upregulated in erlotinib-resistant cells, and knockdown of H19 inhibited cell proliferation, migration and invasion in erlotinib-resistant cells. Erlotinib Hydrochloride 32-41 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32606925-11 2020 Results: H19 was upregulated in erlotinib-resistant cells, and knockdown of H19 inhibited cell proliferation, migration and invasion in erlotinib-resistant cells. Erlotinib Hydrochloride 136-145 H19 imprinted maternally expressed transcript Homo sapiens 76-79 32606925-13 2020 Exosomes containing H19 induced erlotinib resistance of sensitive cells, while knockdown of H19 abolished this effect. Erlotinib Hydrochloride 32-41 H19 imprinted maternally expressed transcript Homo sapiens 20-23 32606925-14 2020 miR-615-3p was a target of H19 and can bind to ATG7. mir-615-3p 0-10 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32606925-15 2020 Exosomal H19 affected erlotinib resistance of erlotinib-resistant NSCLC cells via targeting miR-615-3p to regulate ATG7 expression. Erlotinib Hydrochloride 22-31 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32606925-15 2020 Exosomal H19 affected erlotinib resistance of erlotinib-resistant NSCLC cells via targeting miR-615-3p to regulate ATG7 expression. Erlotinib Hydrochloride 46-55 H19 imprinted maternally expressed transcript Homo sapiens 9-12 32606925-16 2020 In addition, the serum exosomal H19 was upregulated in patients with erlotinib resistance. Erlotinib Hydrochloride 69-78 H19 imprinted maternally expressed transcript Homo sapiens 32-35 32606925-17 2020 Furthermore, downregulated H19 decreased the resistance of tumor cells to erlotinib in vivo. Erlotinib Hydrochloride 74-83 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32606925-18 2020 Conclusion: Our study demonstrated that exosomal H19 facilitated erlotinib resistance in NSCLC via miR-615-3p/ATG7 axis, which might provide a potential target for the diagnosis and treatment of NSCLC. Erlotinib Hydrochloride 65-74 H19 imprinted maternally expressed transcript Homo sapiens 49-52 32362074-6 2020 Chromatin immunoprecipitation and dual luciferase reporter assays were applied to verify H19 transcriptional and posttranscriptional regulation by miR-103a. mir-103a 147-155 H19 imprinted maternally expressed transcript Homo sapiens 89-92 32533641-3 2020 An example of the less well-established pharmacological approach is the calcium-channel blocker gallopamil which in a clinical trial effectively reduced ASM thickness; other agents may act similarly. Calcium 72-79 H19 imprinted maternally expressed transcript Homo sapiens 153-156 32533641-3 2020 An example of the less well-established pharmacological approach is the calcium-channel blocker gallopamil which in a clinical trial effectively reduced ASM thickness; other agents may act similarly. Gallopamil 96-106 H19 imprinted maternally expressed transcript Homo sapiens 153-156 32533641-4 2020 In view of established anti-proliferative properties of the macrolide antibiotic azithromycin, we examined its effects in naive mice and report a reduction in ASM thickness of 29% (p < .01). Macrolides 60-69 H19 imprinted maternally expressed transcript Homo sapiens 159-162 32533641-4 2020 In view of established anti-proliferative properties of the macrolide antibiotic azithromycin, we examined its effects in naive mice and report a reduction in ASM thickness of 29% (p < .01). Azithromycin 81-93 H19 imprinted maternally expressed transcript Homo sapiens 159-162 32533641-8 2020 Findings provide further proof of concept that pharmacological targeting of ASM thickness will be beneficial and may be facilitated by azithromycin, revealing a new mode of action of an existing agent in respiratory medicine. Azithromycin 135-147 H19 imprinted maternally expressed transcript Homo sapiens 76-79 32460893-14 2020 H19 binds directly to miR-140-5p and overexpression of miR-140-5p inhibited odontoblastic differentiation of hDPSCs. mir-140-5p 22-32 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32443594-6 2020 Eosinophils adhesion to hTERT airway smooth muscle (ASM) cells was measured by evaluating their peroxidase activity and viability by annexin V and propidium iodide staining. Propidium 147-163 H19 imprinted maternally expressed transcript Homo sapiens 52-55 32435188-3 2020 Using human airway smooth muscle (ASM) cells and murine precision-cut lung slices, we discovered that pitavastatin significantly inhibited basal-, histamine-, and methacholine (MCh)-induced ASM contraction. pitavastatin 102-114 H19 imprinted maternally expressed transcript Homo sapiens 190-193 32435188-3 2020 Using human airway smooth muscle (ASM) cells and murine precision-cut lung slices, we discovered that pitavastatin significantly inhibited basal-, histamine-, and methacholine (MCh)-induced ASM contraction. Histamine 147-156 H19 imprinted maternally expressed transcript Homo sapiens 190-193 32435188-3 2020 Using human airway smooth muscle (ASM) cells and murine precision-cut lung slices, we discovered that pitavastatin significantly inhibited basal-, histamine-, and methacholine (MCh)-induced ASM contraction. Methacholine Chloride 163-175 H19 imprinted maternally expressed transcript Homo sapiens 190-193 32435188-3 2020 Using human airway smooth muscle (ASM) cells and murine precision-cut lung slices, we discovered that pitavastatin significantly inhibited basal-, histamine-, and methacholine (MCh)-induced ASM contraction. Methacholine Chloride 177-180 H19 imprinted maternally expressed transcript Homo sapiens 190-193 32435188-5 2020 Pitavastatin also potentiated the ASM relaxing effect of a simulated deep breath, a beneficial effect that is notably absent with the beta2-agonist, isoproterenol. pitavastatin 0-12 H19 imprinted maternally expressed transcript Homo sapiens 34-37 32435188-6 2020 Finally, pitavastatin attenuated ASM pro-inflammatory cytokine production in a GGPP-dependent manner. pitavastatin 9-21 H19 imprinted maternally expressed transcript Homo sapiens 33-36 31845415-6 2020 Our results also show that A20 expression was significantly reduced in blood leukocytes and ASM obtained from patients with asthma compared to cells obtained from healthy subjects which was restored after incubation with IRL201104 in vitro, when added alone, or in combination with LPS or TNF-alpha in ASM. IRL 2500 221-230 H19 imprinted maternally expressed transcript Homo sapiens 92-95 32355545-5 2020 To determine the expression of H19 in calcified VSMCs, we induced VSMCs calcification with 10 mM beta-glycerophosphate. beta-glycerophosphoric acid 97-118 H19 imprinted maternally expressed transcript Homo sapiens 31-34 32219038-10 2020 Most importantly, H19 was positively regulated by ICA and H19 depletion could reverse the inhibitory effects of ICA on cell cycle progression and proliferation in PDGF-BB-stimulated RPE cells. icariin 112-115 H19 imprinted maternally expressed transcript Homo sapiens 58-61 32934949-5 2020 The association of plasma level of lipid and homocystine with H19 expression was also considered. Homocystine 45-56 H19 imprinted maternally expressed transcript Homo sapiens 62-65 32934949-8 2020 Additionally, the relative expression level of H19 was directly associated with the plasma homocystine level. Homocystine 91-102 H19 imprinted maternally expressed transcript Homo sapiens 47-50 32096599-3 2020 Furthermore, we explored alterations in DNA methylation profile of imprinting control region at growth-related insulin-like growth factor 2 (IGF2)/H19 locus in twins" white blood cells (WBC), which have been associated earlier with alcohol-induced genotype-specific changes in placental tissue. Alcohols 232-239 H19 imprinted maternally expressed transcript Homo sapiens 147-150 32015047-8 2020 Small-colony variants were selected by tobramycin in ASM(+) and by ciprofloxacin in both media. Tobramycin 39-49 H19 imprinted maternally expressed transcript Homo sapiens 53-56 32219038-10 2020 Most importantly, H19 was positively regulated by ICA and H19 depletion could reverse the inhibitory effects of ICA on cell cycle progression and proliferation in PDGF-BB-stimulated RPE cells. icariin 50-53 H19 imprinted maternally expressed transcript Homo sapiens 18-21 32219038-10 2020 Most importantly, H19 was positively regulated by ICA and H19 depletion could reverse the inhibitory effects of ICA on cell cycle progression and proliferation in PDGF-BB-stimulated RPE cells. icariin 112-115 H19 imprinted maternally expressed transcript Homo sapiens 18-21 32480246-3 2020 One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). NAD 32-35 H19 imprinted maternally expressed transcript Homo sapiens 169-172 32480246-3 2020 One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Cyclic ADP-Ribose 78-95 H19 imprinted maternally expressed transcript Homo sapiens 169-172 32480246-3 2020 One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Calcium 126-133 H19 imprinted maternally expressed transcript Homo sapiens 169-172 32480246-4 2020 Upregulation of CD38 in ASM caused by exposure to cytokines or allergens leads to enhanced calcium mobilization by agonists and the development of airway hyperresponsiveness (AHR) to contractile agonists. Calcium 91-98 H19 imprinted maternally expressed transcript Homo sapiens 24-27 32219038-11 2020 Further mechanical explorations showed that H19 knockdown resulted in alternative expressions levels of cyclin D1, CDK4, CDK6, p21 and p53 under ICA treatment. icariin 145-148 H19 imprinted maternally expressed transcript Homo sapiens 44-47 31953562-10 2020 RESULTS: We identified that H19 and XBP1s were down-regulated in ARPE-19 cells under high-glucose condition, while miR-93 was up-regulated. Glucose 90-97 H19 imprinted maternally expressed transcript Homo sapiens 28-31 32107606-6 2020 RESULTS: Overexpression of H19 in EVT cells increased cell migration and tube formation, while downregulation of H19 in EVT cells decreased cell migration and tube formation. EVT 34-37 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32107606-6 2020 RESULTS: Overexpression of H19 in EVT cells increased cell migration and tube formation, while downregulation of H19 in EVT cells decreased cell migration and tube formation. EVT 120-123 H19 imprinted maternally expressed transcript Homo sapiens 113-116 32107606-8 2020 In addition, we demonstrated the H19/miR-106a-5p/VEGFA regulatory axis in EVT. EVT 74-77 H19 imprinted maternally expressed transcript Homo sapiens 33-36 32107606-10 2020 CONCLUSION: H19/miR-106a-5p/VEGFA axis plays a role in regulating the angiogenic capacity of EVT, which might contribute to idiopathic RM. EVT 93-96 H19 imprinted maternally expressed transcript Homo sapiens 12-15 31887550-3 2020 H19 small interfering RNA (siRNA) (Si-H19) and adenovirus (AD-H19) were used to decrease and increase H19 expression, respectively. Silicon 35-37 H19 imprinted maternally expressed transcript Homo sapiens 0-3 31887550-3 2020 H19 small interfering RNA (siRNA) (Si-H19) and adenovirus (AD-H19) were used to decrease and increase H19 expression, respectively. Silicon 35-37 H19 imprinted maternally expressed transcript Homo sapiens 38-41 31887550-3 2020 H19 small interfering RNA (siRNA) (Si-H19) and adenovirus (AD-H19) were used to decrease and increase H19 expression, respectively. Silicon 35-37 H19 imprinted maternally expressed transcript Homo sapiens 38-41 31887550-3 2020 H19 small interfering RNA (siRNA) (Si-H19) and adenovirus (AD-H19) were used to decrease and increase H19 expression, respectively. Silicon 35-37 H19 imprinted maternally expressed transcript Homo sapiens 38-41 31887550-6 2020 Si-H19 significantly downregulated miR22-5p and upregulated miR675-5p expression; Si-H19 decreased the protein and mRNA expression of VDR and decreased the cytokine and mRNA levels of interleukin-17A (IL-17A) and IL-23. Silicon 0-2 H19 imprinted maternally expressed transcript Homo sapiens 3-6 31887550-6 2020 Si-H19 significantly downregulated miR22-5p and upregulated miR675-5p expression; Si-H19 decreased the protein and mRNA expression of VDR and decreased the cytokine and mRNA levels of interleukin-17A (IL-17A) and IL-23. Silicon 82-84 H19 imprinted maternally expressed transcript Homo sapiens 85-88 31940218-6 2020 Exposure of hASM to tunicamycin was used as a positive control. Tunicamycin 20-31 H19 imprinted maternally expressed transcript Homo sapiens 12-16 31940218-9 2020 We found that exposure of hASM cells to tunicamycin activated all three ER stress pathways. Tunicamycin 40-51 H19 imprinted maternally expressed transcript Homo sapiens 26-30 31953562-14 2020 CONCLUSIONS: H19 played an important role in regulating inflammatory processes in retinal endothelial cells under high-glucose condition through modulating miR-93/XBP1s axis. Glucose 119-126 H19 imprinted maternally expressed transcript Homo sapiens 13-16 31747299-2 2020 We have previously shown that TMEM16A antagonists such as benzbromarone relax ASM and have proposed TMEM16A antagonists as novel therapies for asthma treatment. Benzbromarone 58-71 H19 imprinted maternally expressed transcript Homo sapiens 78-81 31468534-3 2020 Real-time polymerase chain reaction and western-blot analysis were used to study the effect of CUR or 1,25-dihydroxyvitamin D (1,25(OH)2 D3 ) on the expression of H19, miR-675, and VDR. 1,25-dihydroxyvitamin D 102-125 H19 imprinted maternally expressed transcript Homo sapiens 163-166 31468534-3 2020 Real-time polymerase chain reaction and western-blot analysis were used to study the effect of CUR or 1,25-dihydroxyvitamin D (1,25(OH)2 D3 ) on the expression of H19, miR-675, and VDR. Calcitriol 127-139 H19 imprinted maternally expressed transcript Homo sapiens 163-166 31747299-5 2020 The TMEM16A agonist Eact induced a significant contraction of human ASM and guinea pig tracheal rings in an ex vivo organ bath model. (3,4,5-trimethoxy-N-(2-methoxyethyl)-N-(4-phenyl-2-thiazolyl)benzamide 20-24 H19 imprinted maternally expressed transcript Homo sapiens 68-71 31747299-11 2020 Eact caused an increase in intracellular calcium in human ASM cells that was completely attenuated by pretreatment with benzbromarone. Calcium 41-48 H19 imprinted maternally expressed transcript Homo sapiens 58-61 31747299-11 2020 Eact caused an increase in intracellular calcium in human ASM cells that was completely attenuated by pretreatment with benzbromarone. Benzbromarone 120-133 H19 imprinted maternally expressed transcript Homo sapiens 58-61 31747299-12 2020 Eact acutely depolarized the plasma membrane potential of ASM cells, which was attenuated by benzbromarone or nifedipine. Benzbromarone 93-106 H19 imprinted maternally expressed transcript Homo sapiens 58-61 31747299-12 2020 Eact acutely depolarized the plasma membrane potential of ASM cells, which was attenuated by benzbromarone or nifedipine. Nifedipine 110-120 H19 imprinted maternally expressed transcript Homo sapiens 58-61 31663716-8 2019 The constructed maps were generally consistent with the corresponding isothermal section of the Fe-Cr-Ni ternary alloy system in the ASM Alloy Phase Diagram Database except the inexistence of the sigma phase under insufficient annealing. fe-cr-ni 96-104 H19 imprinted maternally expressed transcript Homo sapiens 133-136 32356434-1 2020 OBJECTIVES: In the present study, cellular or exosomal expression of H19, an oncofetal lncRNA gene, was evaluated during androgen stimulation via dihydrotestosterone (DHT) or AR blockage via enzalutamide in cultured hormone-sensitive Pca cells which overexpres AR (LNCaP-AR+). Dihydrotestosterone 146-165 H19 imprinted maternally expressed transcript Homo sapiens 69-72 32356434-1 2020 OBJECTIVES: In the present study, cellular or exosomal expression of H19, an oncofetal lncRNA gene, was evaluated during androgen stimulation via dihydrotestosterone (DHT) or AR blockage via enzalutamide in cultured hormone-sensitive Pca cells which overexpres AR (LNCaP-AR+). Dihydrotestosterone 167-170 H19 imprinted maternally expressed transcript Homo sapiens 69-72 32356434-1 2020 OBJECTIVES: In the present study, cellular or exosomal expression of H19, an oncofetal lncRNA gene, was evaluated during androgen stimulation via dihydrotestosterone (DHT) or AR blockage via enzalutamide in cultured hormone-sensitive Pca cells which overexpres AR (LNCaP-AR+). enzalutamide 191-203 H19 imprinted maternally expressed transcript Homo sapiens 69-72 32356434-5 2020 METHODS: Cells were treated with DHT (10 nM) and/or enzalutamide (10 uM) for 24 h. Cellular and exosomal expression of H19 was investigated using a quantitative polymerase chain reaction assay. Dihydrotestosterone 33-36 H19 imprinted maternally expressed transcript Homo sapiens 119-122 32356434-7 2020 AR blockage using enzalutamide restored DHT effect and we found increased H19 expression (<= 2.5-fold, p < 0.05) upon the combined use of DHT and enzalutamide compared to control cells. Dihydrotestosterone 138-141 H19 imprinted maternally expressed transcript Homo sapiens 74-77 32356434-7 2020 AR blockage using enzalutamide restored DHT effect and we found increased H19 expression (<= 2.5-fold, p < 0.05) upon the combined use of DHT and enzalutamide compared to control cells. enzalutamide 146-158 H19 imprinted maternally expressed transcript Homo sapiens 74-77 32356434-8 2020 Similar to its cellular effect, DHT treatment also led to declined exosomal expression of H19 (<= 3-fold, p < 0.0001). Dihydrotestosterone 32-35 H19 imprinted maternally expressed transcript Homo sapiens 90-93 32356434-9 2020 Restorative effect of enzalutamide on decreased H19 expression induced by androgen stimulation was not observed in exosomes. enzalutamide 22-34 H19 imprinted maternally expressed transcript Homo sapiens 48-51 31809000-4 2020 We found that H19 was up-regulated in oleic acid-induced steatosis and during the development of high-fat diet (HFD)-induced NAFLD. Oleic Acids 38-48 H19 imprinted maternally expressed transcript Homo sapiens 14-17 31809000-8 2020 Furthermore, H19-induced lipid accumulation was effectively inhibited by PI3K/mTOR inhibitor PF-04691502. 2-amino-8-(4-(2-hydroxyethoxy)cyclohexyl)-6-(6-methoxypyridin-3-yl)-4-methylpyrido(2,3-d)pyrimidin-7(8H)-one 93-104 H19 imprinted maternally expressed transcript Homo sapiens 13-16 31705929-6 2020 LncRNA H19 positively correlated with CD68+ TAMs in situ. Tams1 antigen 44-48 H19 imprinted maternally expressed transcript Homo sapiens 7-10 31705929-7 2020 TAMs-induced lncRNA H19 promotes HCC aggressiveness via triggering and activating the miR-193b/MAPK1 axis, mediates the crosstalk between HCC and immunological microenvironment, and causes poor clinical outcomes. Tams1 antigen 0-4 H19 imprinted maternally expressed transcript Homo sapiens 20-23 31918667-12 2020 Moreover, the expression of miR-19b-3p was inhibited, while H19 elvated in 17beta-estradiol (E2) treated BMSCs in a dose-dependent manner. Estradiol 75-91 H19 imprinted maternally expressed transcript Homo sapiens 60-63 31735555-10 2019 Moreover, H19 downregulation inhibited HMGB1, TLR4 and NF-kappaB expression and suppressed CaOx nephrocalcinosis-induced renal tubular epithelial cell injury, NADPH oxidase, and oxidative stress in vivo and in vitro. NADP 159-164 H19 imprinted maternally expressed transcript Homo sapiens 10-13 31735555-12 2019 INTERPRETATION: We determined that H19 might serve as a facilitator in the process of CaOx nephrocalcinosis-induced oxidative stress and renal tubular epithelial cell injury, and we revealed that the interaction between H19 and miR-216b could exert its effect via the HMGB1/TLR4/NF-kappaB pathway. Calcium Oxalate 86-90 H19 imprinted maternally expressed transcript Homo sapiens 35-38 31735555-0 2019 H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway. Calcium Oxalate 12-27 H19 imprinted maternally expressed transcript Homo sapiens 0-3 31369093-8 2019 Cabergoline increased H19 expression and played a synergic therapeutic effect with exosomal H19. Cabergoline 0-11 H19 imprinted maternally expressed transcript Homo sapiens 22-25 31735555-2 2019 A recent genome-wide gene expression profile analysis of Randall"s plaques in CaOx stone patients revealed that the expression of the long noncoding RNA H19 was significantly upregulated. Calcium Oxalate 78-82 H19 imprinted maternally expressed transcript Homo sapiens 153-156 31735555-10 2019 Moreover, H19 downregulation inhibited HMGB1, TLR4 and NF-kappaB expression and suppressed CaOx nephrocalcinosis-induced renal tubular epithelial cell injury, NADPH oxidase, and oxidative stress in vivo and in vitro. Calcium Oxalate 91-95 H19 imprinted maternally expressed transcript Homo sapiens 10-13 31858547-1 2019 OBJECTIVE: To illustrate the role of FOXF2 in the aggravation of the progression of non-small cell lung cancer (NSCLC) by targeting long non-coding RNA (lncRNA) H19 to down-regulate the gene of phosphate and tensin homolog deleted on chromosome ten (PTEN). Phosphates 194-203 H19 imprinted maternally expressed transcript Homo sapiens 161-164 31638183-0 2019 In vitro and in vivo studies on the association of long non-coding RNAs H19 and urothelial cancer associated 1 with the susceptibility to 5-fluorouracil in rectal cancer. Fluorouracil 138-152 H19 imprinted maternally expressed transcript Homo sapiens 72-75 31638183-4 2019 Bioinformatic analysis identified H19 and urothelial cancer associated 1 (UCA1) as candidate biomarkers for 5FU susceptibility. Fluorouracil 108-111 H19 imprinted maternally expressed transcript Homo sapiens 34-37 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 64-67 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31638183-6 2019 The ratios of changes of H19 and UCA1 expression in response to 5FU were low in cells resistant to 5FU, whereas ratios were high in cells susceptible to 5FU. Fluorouracil 99-102 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31638183-11 2019 The increase in H19 and UCA1 expression may represent the response to impaired cell cycle in cells susceptible to 5FU. Fluorouracil 114-117 H19 imprinted maternally expressed transcript Homo sapiens 16-19 31638183-12 2019 Our results indicate that changes in H19 and UCA1 expression may be considered for predicting the susceptibility to 5FU-based NAC in rectal cancer. Fluorouracil 116-119 H19 imprinted maternally expressed transcript Homo sapiens 37-40 31369093-8 2019 Cabergoline increased H19 expression and played a synergic therapeutic effect with exosomal H19. Cabergoline 0-11 H19 imprinted maternally expressed transcript Homo sapiens 92-95 31411061-7 2019 By contrast, carbachol-induced contraction of the ASM derived from Pkd2SM-CKO mice was significantly reduced compared with that in wild-type mice. Carbachol 13-22 H19 imprinted maternally expressed transcript Homo sapiens 50-53 31549747-5 2019 Remarkable decrease of methylation in imprinted gene H19 and increased apoptosis was observed in 5 and 50 microM RG108-treated cells. RG108 113-118 H19 imprinted maternally expressed transcript Homo sapiens 53-56 31298967-1 2019 Plant activators, including acibenzolar-S-methyl (ASM), are chemical compounds that stimulate plant defense responses to pathogens. S-methyl benzo(1,2,3)thiadiazole-7-carbothioate 28-48 H19 imprinted maternally expressed transcript Homo sapiens 50-53 31618367-0 2019 Schizandrin A exerts anti-tumor effects on A375 cells by down-regulating H19. schizandrin A 0-13 H19 imprinted maternally expressed transcript Homo sapiens 73-76 31618367-14 2019 Overexpression of H19 blockaded the inhibitory effects of SchA on A375 cells. schizandrin A 58-62 H19 imprinted maternally expressed transcript Homo sapiens 18-21 31618367-16 2019 SchA inhibited A375 cell growth, migration, and the PI3K/AKT pathway through down-regulating H19. schizandrin A 0-4 H19 imprinted maternally expressed transcript Homo sapiens 93-96 31411527-8 2019 Furthermore, H19 was also verified to stimulate the activity of endometrial cancer with AXL inhibitor BGB324 in vitro and in vivo. bemcentinib 102-108 H19 imprinted maternally expressed transcript Homo sapiens 13-16 31827510-10 2019 These data suggest a potential role for both H19 and MALAT1 lncRNAs as prognostic biomarker for the clinical selection of the best candidate to first-line treatment with imatinib. Imatinib Mesylate 170-178 H19 imprinted maternally expressed transcript Homo sapiens 45-48 31737629-7 2019 We found that positive modulation of miR29b and inhibition of H19 and VEGFA significantly attenuates high glucose-induced endothelial inflammation and oxidative stress. Glucose 106-113 H19 imprinted maternally expressed transcript Homo sapiens 62-65 31737629-9 2019 We conclude that H19 suppression protects the endothelium against high glucose-induced inflammation and oxidative stress in endothelial cells by upregulation of miR-29b and downregulation of VEGFA through AKT/eNOS signal pathway activation. Glucose 71-78 H19 imprinted maternally expressed transcript Homo sapiens 17-20 31362245-6 2019 The results showed that the expression of H19 and HE4 was down-regulated by high glucose and further, alpha-Mangostin restored the high glucose-induced inhibition of H19 and HE4 expression. Glucose 81-88 H19 imprinted maternally expressed transcript Homo sapiens 42-45 31362245-6 2019 The results showed that the expression of H19 and HE4 was down-regulated by high glucose and further, alpha-Mangostin restored the high glucose-induced inhibition of H19 and HE4 expression. mangostin 102-117 H19 imprinted maternally expressed transcript Homo sapiens 42-45 31362245-6 2019 The results showed that the expression of H19 and HE4 was down-regulated by high glucose and further, alpha-Mangostin restored the high glucose-induced inhibition of H19 and HE4 expression. mangostin 102-117 H19 imprinted maternally expressed transcript Homo sapiens 166-169 31362245-6 2019 The results showed that the expression of H19 and HE4 was down-regulated by high glucose and further, alpha-Mangostin restored the high glucose-induced inhibition of H19 and HE4 expression. Glucose 136-143 H19 imprinted maternally expressed transcript Homo sapiens 42-45 31362245-6 2019 The results showed that the expression of H19 and HE4 was down-regulated by high glucose and further, alpha-Mangostin restored the high glucose-induced inhibition of H19 and HE4 expression. Glucose 136-143 H19 imprinted maternally expressed transcript Homo sapiens 166-169 31362245-7 2019 Further examination demonstrated that the modulation of the H19 and HE4 expression affected the function of alpha-Mangostin in hyperglycemia. mangostin 108-123 H19 imprinted maternally expressed transcript Homo sapiens 60-63 31362245-9 2019 Finally, we showed that H19 exerted its function via the modulation of H19/miR-140/HE4 in hyperglycemia with alpha-Mangostin. mangostin 109-124 H19 imprinted maternally expressed transcript Homo sapiens 24-27 31362245-9 2019 Finally, we showed that H19 exerted its function via the modulation of H19/miR-140/HE4 in hyperglycemia with alpha-Mangostin. mangostin 109-124 H19 imprinted maternally expressed transcript Homo sapiens 71-74 31411061-8 2019 In addition, relaxation of the carbachol-precontracted ASM by isoprenaline, a beta-adrenergic receptor agonist that acts through the cAMP/adenylyl cyclase pathway, was also significantly attenuated in Pkd2SM-CKO mice compared with that in wild-type mice. Carbachol 31-40 H19 imprinted maternally expressed transcript Homo sapiens 55-58 31411061-8 2019 In addition, relaxation of the carbachol-precontracted ASM by isoprenaline, a beta-adrenergic receptor agonist that acts through the cAMP/adenylyl cyclase pathway, was also significantly attenuated in Pkd2SM-CKO mice compared with that in wild-type mice. Isoproterenol 62-74 H19 imprinted maternally expressed transcript Homo sapiens 55-58 31411061-8 2019 In addition, relaxation of the carbachol-precontracted ASM by isoprenaline, a beta-adrenergic receptor agonist that acts through the cAMP/adenylyl cyclase pathway, was also significantly attenuated in Pkd2SM-CKO mice compared with that in wild-type mice. Cyclic AMP 133-137 H19 imprinted maternally expressed transcript Homo sapiens 55-58 31432188-0 2019 The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis. Oxaliplatin 81-92 H19 imprinted maternally expressed transcript Homo sapiens 29-32 31120314-7 2019 Current smoking women presented a higher odds ratio (OR) for accelerated loss of ASM than nonsmoking individuals after adjusting for age, body mass index, exercise, caloric intake, alcohol consumption, menopausal state, and diabetes mellitus (DM) (OR 3.53, confidence interval [95% CI] 1.28-9.74, p = 0.015). Alcohols 181-188 H19 imprinted maternally expressed transcript Homo sapiens 81-84 31432188-0 2019 The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis. Irinotecan 96-106 H19 imprinted maternally expressed transcript Homo sapiens 29-32 30536718-6 2019 Moreover, stimulation of ASM with PGE2 did not establish a positive, receptor-mediated, feedback loop, as mRNA expression for EP2 and EP4 receptors were not upregulated and receptor antagonists were without effect. Dinoprostone 34-38 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31020694-6 2019 We used human CC cell line JEG-3 to establish cell lines resistant to methotrexate and 5-fluorouracil (JEG-3/MTX and JEG-3/5-FU) and detected the expression of H19 in JEG-3, JEG-3/MTX, JEG-3/5-FU cells, JEG-3 with MTX, and JEG-3 with 5-FU. Methotrexate 180-183 H19 imprinted maternally expressed transcript Homo sapiens 160-163 31020694-6 2019 We used human CC cell line JEG-3 to establish cell lines resistant to methotrexate and 5-fluorouracil (JEG-3/MTX and JEG-3/5-FU) and detected the expression of H19 in JEG-3, JEG-3/MTX, JEG-3/5-FU cells, JEG-3 with MTX, and JEG-3 with 5-FU. Methotrexate 180-183 H19 imprinted maternally expressed transcript Homo sapiens 160-163 31020694-7 2019 We found that the expression of H19 in the JEG-3/MTX and JEG-3/5-FU cells were significantly higher than that in JEG-3 cells. Methotrexate 49-52 H19 imprinted maternally expressed transcript Homo sapiens 32-35 31020694-8 2019 JEG-3 cells were treated with MTX or 5-FU for and quantitative real-time polymerase chain reaction assay revealed that H19 messenger RNA expression increased. Methotrexate 30-33 H19 imprinted maternally expressed transcript Homo sapiens 119-122 31020694-8 2019 JEG-3 cells were treated with MTX or 5-FU for and quantitative real-time polymerase chain reaction assay revealed that H19 messenger RNA expression increased. Fluorouracil 37-41 H19 imprinted maternally expressed transcript Homo sapiens 119-122 31020694-9 2019 Furthermore, after H19 was knocked out, the drug resistance index of the JEG-3/MTX and JEG-3/5-FU cells decreased; the proliferation, migration, and invasion ability diminished significantly; and apoptosis increased significantly. Methotrexate 79-82 H19 imprinted maternally expressed transcript Homo sapiens 19-22 31391459-0 2019 Correction: H19 lncRNA alters methylation and expression of Hnf4alpha in the liver of metformin-exposed fetuses. Metformin 86-95 H19 imprinted maternally expressed transcript Homo sapiens 12-15 31336636-7 2019 The results showed 1-OHPH is specifically correlated with CpG4 and CpG6 of the imprinted gene H19, CpG1 and CpG2 of PEG3, and CpG2 of MEG3; whereas 1-OHP is positively correlated with PEG3 at CpG1. Oxaliplatin 19-24 H19 imprinted maternally expressed transcript Homo sapiens 94-97 31336636-8 2019 Multivariate regression model analysis confirmed that 1-OHPH and 1-OHP are independent risk factors for the methylation of H19. -ohph 55-60 H19 imprinted maternally expressed transcript Homo sapiens 123-126 30536718-4 2019 Using primary human airway smooth muscle (ASM) cells, we first focussed on the PGE2 -induced production of two cAMP-dependent proinflammatory mediators: interleukin 6 (IL-6) and cyclo-oxygenase 2 production. Dinoprostone 79-83 H19 imprinted maternally expressed transcript Homo sapiens 42-45 31512410-4 2019 Exposure to TNFalpha increased maximum ASM force in response to acetylcholine (Ach), with an increase in ACh sensitivity (hyperreactivity), as reflected by a leftward shift in the dose-response curve (EC50 ). Acetylcholine 64-77 H19 imprinted maternally expressed transcript Homo sapiens 39-42 31512410-4 2019 Exposure to TNFalpha increased maximum ASM force in response to acetylcholine (Ach), with an increase in ACh sensitivity (hyperreactivity), as reflected by a leftward shift in the dose-response curve (EC50 ). Acetylcholine 79-82 H19 imprinted maternally expressed transcript Homo sapiens 39-42 30982795-8 2019 Moreover, lncRNA H19 expression was positively correlated with fasting plasma glucose levels; this was the case with both raw data, and after adjustment for age and BMI in the PCOS group. Glucose 78-85 H19 imprinted maternally expressed transcript Homo sapiens 17-20 31340867-4 2019 Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer. Tamoxifen 56-65 H19 imprinted maternally expressed transcript Homo sapiens 30-33 31340867-5 2019 METHODS: Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Tamoxifen 66-75 H19 imprinted maternally expressed transcript Homo sapiens 59-62 31340867-6 2019 Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Tamoxifen 55-64 H19 imprinted maternally expressed transcript Homo sapiens 13-16 31340867-8 2019 Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19. Tamoxifen 164-173 H19 imprinted maternally expressed transcript Homo sapiens 198-201 31340867-9 2019 RESULTS: In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Tamoxifen 96-105 H19 imprinted maternally expressed transcript Homo sapiens 59-62 31340867-9 2019 RESULTS: In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Tamoxifen 208-217 H19 imprinted maternally expressed transcript Homo sapiens 59-62 31340867-9 2019 RESULTS: In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Tamoxifen 208-217 H19 imprinted maternally expressed transcript Homo sapiens 176-179 31340867-10 2019 Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Tamoxifen 72-81 H19 imprinted maternally expressed transcript Homo sapiens 26-29 31340867-12 2019 Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Tamoxifen 45-54 H19 imprinted maternally expressed transcript Homo sapiens 33-36 31340867-12 2019 Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Tamoxifen 90-99 H19 imprinted maternally expressed transcript Homo sapiens 33-36 31340867-16 2019 CONCLUSIONS: Our findings demonstrate that H19 induces autophagy activation via the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer. Tamoxifen 132-141 H19 imprinted maternally expressed transcript Homo sapiens 43-46 31340867-16 2019 CONCLUSIONS: Our findings demonstrate that H19 induces autophagy activation via the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer. Tamoxifen 132-141 H19 imprinted maternally expressed transcript Homo sapiens 84-87 31336636-5 2019 The results from the correlation analysis using seven OH-PAHs and the average methylation levels of the imprinting genes H19, PEG3, and MEG3 indicated that 1-OHPH is positively correlated with H19/PEG3 methylation levels. oh-pahs 54-61 H19 imprinted maternally expressed transcript Homo sapiens 121-124 31336636-5 2019 The results from the correlation analysis using seven OH-PAHs and the average methylation levels of the imprinting genes H19, PEG3, and MEG3 indicated that 1-OHPH is positively correlated with H19/PEG3 methylation levels. oh-pahs 54-61 H19 imprinted maternally expressed transcript Homo sapiens 193-196 31336636-5 2019 The results from the correlation analysis using seven OH-PAHs and the average methylation levels of the imprinting genes H19, PEG3, and MEG3 indicated that 1-OHPH is positively correlated with H19/PEG3 methylation levels. 1-ohph 156-162 H19 imprinted maternally expressed transcript Homo sapiens 121-124 31336636-5 2019 The results from the correlation analysis using seven OH-PAHs and the average methylation levels of the imprinting genes H19, PEG3, and MEG3 indicated that 1-OHPH is positively correlated with H19/PEG3 methylation levels. 1-ohph 156-162 H19 imprinted maternally expressed transcript Homo sapiens 193-196 31336636-7 2019 The results showed 1-OHPH is specifically correlated with CpG4 and CpG6 of the imprinted gene H19, CpG1 and CpG2 of PEG3, and CpG2 of MEG3; whereas 1-OHP is positively correlated with PEG3 at CpG1. 1-ohph 19-25 H19 imprinted maternally expressed transcript Homo sapiens 94-97 31082440-6 2019 15N NMR spectra indicate that removal of the second histidine converted the protonation and tautomeric equilibria of H19 to be similar to the H37 behavior in AM2, indicating that the peripheral H27 is indeed the origin of the low pKa"s of H19 in wild-type BM2. 15n 0-3 H19 imprinted maternally expressed transcript Homo sapiens 239-242 30270743-6 2019 The data further indicated that the patients who presented with the majority of the CpG sites in the H19 DMR region that were lower methylated were those in the OAZ group. aspartylmethionylarginine 105-108 H19 imprinted maternally expressed transcript Homo sapiens 101-104 31082440-6 2019 15N NMR spectra indicate that removal of the second histidine converted the protonation and tautomeric equilibria of H19 to be similar to the H37 behavior in AM2, indicating that the peripheral H27 is indeed the origin of the low pKa"s of H19 in wild-type BM2. 15n 0-3 H19 imprinted maternally expressed transcript Homo sapiens 117-120 31082440-6 2019 15N NMR spectra indicate that removal of the second histidine converted the protonation and tautomeric equilibria of H19 to be similar to the H37 behavior in AM2, indicating that the peripheral H27 is indeed the origin of the low pKa"s of H19 in wild-type BM2. Histidine 52-61 H19 imprinted maternally expressed transcript Homo sapiens 117-120 31082440-6 2019 15N NMR spectra indicate that removal of the second histidine converted the protonation and tautomeric equilibria of H19 to be similar to the H37 behavior in AM2, indicating that the peripheral H27 is indeed the origin of the low pKa"s of H19 in wild-type BM2. Histidine 52-61 H19 imprinted maternally expressed transcript Homo sapiens 239-242 31082440-9 2019 The proton relay between H19 and H27 is likely mediated by the intervening gating tryptophan through cation-pi interactions. Tryptophan 82-92 H19 imprinted maternally expressed transcript Homo sapiens 25-28 31247032-14 2019 Furthermore, we demonstrated that miR-19 contributed to the promoting effects of HMGB1 on ASM cells by targeting PTEN 3"-UTR. mir-19 34-40 H19 imprinted maternally expressed transcript Homo sapiens 90-93 31196153-10 2019 The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. r 45-46 H19 imprinted maternally expressed transcript Homo sapiens 22-25 31014672-10 2019 Moreover, miR-3619-5p overexpression significantly attenuated the LINC00882-induced promotion effect on PDGF-induced cell proliferation and Wnt/beta-catenin signaling in fetal ASM cells. mir-3619-5p 10-21 H19 imprinted maternally expressed transcript Homo sapiens 176-179 31173296-8 2019 The inhibitory effects of downregulation of H19 on glioma cell proliferation, invasion, and migration were reversed by SKL2001 via the activation of the Wnt/beta-catenin signal pathway, which was further enhanced by inhibition of the Wnt/beta-catenin signal pathway by XAV939. 5-furan-2yl-isoxazole-3-carboxylic acid (3-imidazol-1yl-propyl)-amide 119-126 H19 imprinted maternally expressed transcript Homo sapiens 44-47 30659641-0 2019 Progesterone ameliorates the endometrial polyp by modulating the signaling pathway of Wnt and beta-catenin via regulating the expression of H19 and miR-152. Progesterone 0-12 H19 imprinted maternally expressed transcript Homo sapiens 140-143 30659641-7 2019 RESULTS: Progesterone dose-dependently increased the H19 expression level through driving the promoter efficiency of H19. Progesterone 9-21 H19 imprinted maternally expressed transcript Homo sapiens 53-56 30659641-7 2019 RESULTS: Progesterone dose-dependently increased the H19 expression level through driving the promoter efficiency of H19. Progesterone 9-21 H19 imprinted maternally expressed transcript Homo sapiens 117-120 31217890-5 2019 MiR-138 was downregulated in breast cancer tissues and negatively correlated with the expression of H19 and SOX4. mir-138 0-7 H19 imprinted maternally expressed transcript Homo sapiens 100-103 31217890-8 2019 Additionally, miR-138 was identified as a direct target of H19 and SOX4; overexpression of miR-138 inhibited the proliferation, invasion and migration of MDA-MB-231 and MCF-7 cells, but promoted apoptosis, which were abrogated by SOX4 overexpression. mir-138 14-21 H19 imprinted maternally expressed transcript Homo sapiens 59-62 31217890-8 2019 Additionally, miR-138 was identified as a direct target of H19 and SOX4; overexpression of miR-138 inhibited the proliferation, invasion and migration of MDA-MB-231 and MCF-7 cells, but promoted apoptosis, which were abrogated by SOX4 overexpression. mir-138 91-98 H19 imprinted maternally expressed transcript Homo sapiens 59-62 31217890-10 2019 In addition, miR-138 overexpression reversed the effects of H19 in breast cancer cells; silencing of H19 inhibited tumor growth and downregulate EMT markers in vivo. mir-138 13-20 H19 imprinted maternally expressed transcript Homo sapiens 60-63 31082282-10 2019 DISCUSSION: The differential regulation of a set of imprinted genes, particularly DLX5, H19, and NDN, in association with prenatal Cd exposure may be involved in overall developmental toxicity, and some imprinted genes may respond to Cd exposure in a manner that is specific to infant gender. Cadmium 131-133 H19 imprinted maternally expressed transcript Homo sapiens 88-91 31082282-10 2019 DISCUSSION: The differential regulation of a set of imprinted genes, particularly DLX5, H19, and NDN, in association with prenatal Cd exposure may be involved in overall developmental toxicity, and some imprinted genes may respond to Cd exposure in a manner that is specific to infant gender. Cadmium 234-236 H19 imprinted maternally expressed transcript Homo sapiens 88-91 31902860-11 2019 After adjusting for multiple factors, serum 25(OH)D was positively associated with grip strength (beta=0.18, p=0.009), ASM (beta=0.14, p<0.001), and RSMI (beta=0.07, p<0.001); 25(OH)D<20 ng/mL was significantly associated with low grip strength (OR=2.97, 95% CI: 1.17-7.55), and low SMM (OR=2.73, 95% CI: 1.15-6.45). 25(oh)d 44-51 H19 imprinted maternally expressed transcript Homo sapiens 119-122 30359078-5 2019 We also assessed isoproterenol responses in maximally methacholine-contracted ASM. Isoproterenol 17-30 H19 imprinted maternally expressed transcript Homo sapiens 78-81 30359078-5 2019 We also assessed isoproterenol responses in maximally methacholine-contracted ASM. Methacholine Chloride 54-66 H19 imprinted maternally expressed transcript Homo sapiens 78-81 30359078-11 2019 Indeed, the percentage of relaxation measured at maximal isoproterenol concentrations in the CF ASM was significantly lower after incubation with IL-13 (46.0% +- 6.7% relaxation) than without IL-13 (74.0% +- 7.7% relaxation, P = 0.018). Isoproterenol 57-70 H19 imprinted maternally expressed transcript Homo sapiens 96-99 30192003-0 2019 Long noncoding RNA H19 participates in metformin-mediated inhibition of gastric cancer cell invasion. Metformin 39-48 H19 imprinted maternally expressed transcript Homo sapiens 19-22 30192003-5 2019 We found that lncRNA H19 was greatly downregulated in gastric cancer cells treated with metformin using lncRNA microassays. Metformin 88-97 H19 imprinted maternally expressed transcript Homo sapiens 21-24 30192003-6 2019 Based on bioinformatics analyses of the Oncomine and The Cancer Genome Atlas databases, H19 is shown to be overexpressed in gastric cancer tissues, with increased expression of H19 relating to advanced pathological tumor stage and pathological tumor node metastasis stage, indicating that H19 may be associated with the invasive ability of gastric cancer. oncomine 40-48 H19 imprinted maternally expressed transcript Homo sapiens 88-91 30192003-9 2019 In summary, metformin has a profound antitumor effect on gastric cancer cells, and H19 is a key component in the process of metformin suppressing gastric cancer cell invasion. Metformin 124-133 H19 imprinted maternally expressed transcript Homo sapiens 83-86 30612136-6 2019 METHODS: H19 was overexpressed or silenced in human retinal endothelial cells exposed to various glucose levels. Glucose 97-104 H19 imprinted maternally expressed transcript Homo sapiens 9-12 30672383-0 2019 Polymorphisms in IGF2/H19 gene locus are associated with platinum-based chemotherapeutic response in Chinese patients with epithelial ovarian cancer. Platinum 57-65 H19 imprinted maternally expressed transcript Homo sapiens 22-25 30672383-1 2019 AIM: The present study aimed to assess the association between IGF2/H19 genetic variants and susceptibility to platinum-based chemotherapy in epithelial ovarian cancer (EOC). Platinum 111-119 H19 imprinted maternally expressed transcript Homo sapiens 68-71 30502591-6 2019 RESULTS: Women using hormonal contraception with the combination of ethinyl estradiol + progestogen had significantly lower mean ASM (18.0), RSMI (6.5), TLM (40.8) (p < 0.01) and GS (34.6) (p < 0.001) compared to the women not using hormonal contraception with mean values of ASM (18.8), RSMI (6.7), TLM (42.6) and GS (36.9). Ethinyl Estradiol 68-85 H19 imprinted maternally expressed transcript Homo sapiens 129-132 30502591-6 2019 RESULTS: Women using hormonal contraception with the combination of ethinyl estradiol + progestogen had significantly lower mean ASM (18.0), RSMI (6.5), TLM (40.8) (p < 0.01) and GS (34.6) (p < 0.001) compared to the women not using hormonal contraception with mean values of ASM (18.8), RSMI (6.7), TLM (42.6) and GS (36.9). Ethinyl Estradiol 68-85 H19 imprinted maternally expressed transcript Homo sapiens 282-285 30728351-0 2019 LncRNA H19 overexpression induces bortezomib resistance in multiple myeloma by targeting MCL-1 via miR-29b-3p. Bortezomib 34-44 H19 imprinted maternally expressed transcript Homo sapiens 7-10 30728351-7 2019 On the basis of these previous findings, the present study was intended to explore the biological function of H19, interactions between the downstream target genes, and the effect of H19 on BTZ resistance of myeloma cells. btz 190-193 H19 imprinted maternally expressed transcript Homo sapiens 183-186 30728351-8 2019 In addition, in vivo experiments we have also confirmed that H19 promoted tumor growth and may develop resistance to bortezomib partly. Bortezomib 117-127 H19 imprinted maternally expressed transcript Homo sapiens 61-64 30728351-9 2019 It was found that H19 reduced cell sensitivity to the chemotherapeutic drug BTZ by working as a miRNA sponge to inhibit the expression of miR-29b-3p, enhance MCL-1 transcriptional translation and inhibit apoptosis. btz 76-79 H19 imprinted maternally expressed transcript Homo sapiens 18-21 32328568-2 2019 This salutary effect of a DI is proposed to be mediated, at least partially, by momentarily increasing the operating length of airway smooth muscle (ASM). di 26-28 H19 imprinted maternally expressed transcript Homo sapiens 149-152 32328568-8 2019 A rough estimated range of ASM strains is provided for the purpose of guiding future in vitro studies that aim at quantifying the regulatory effect of DI on ASM contractility. di 151-153 H19 imprinted maternally expressed transcript Homo sapiens 27-30 32328568-8 2019 A rough estimated range of ASM strains is provided for the purpose of guiding future in vitro studies that aim at quantifying the regulatory effect of DI on ASM contractility. di 151-153 H19 imprinted maternally expressed transcript Homo sapiens 157-160 32699838-6 2019 Recent data indicate that VSELs expand in vivo and in vitro after reestablishment of somatic imprinting at the Igf2-H19 locus by nicotinamide treatment in response to stimulation by pituitary gonadotrophins (follicle stimulating factor, luteinizing hormone and prolactin) and gonadal androgens and estrogens. Niacinamide 129-141 H19 imprinted maternally expressed transcript Homo sapiens 116-119 30240970-0 2018 Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin. Melatonin 111-120 H19 imprinted maternally expressed transcript Homo sapiens 27-30 30619763-7 2018 Pterostilbene increased the expression of the lncRNAs MEG3, TUG1, H19, and DICER1-AS1 whereas the expression of LINC01121, PTTG3P, and HOTAIR declined. pterostilbene 0-13 H19 imprinted maternally expressed transcript Homo sapiens 66-69 30619763-8 2018 Knockdown of lncRNA H19 resulted in a reduction of the cell invasion, with the cells becoming more sensitive to pterostilbene therapy. pterostilbene 112-125 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30576305-6 2018 RESULTS Serum H19 was little influenced by the treatment of RNase A alone but was dramatically downregulated when treated with RNase A and Triton x100 simultaneously. Octoxynol 139-150 H19 imprinted maternally expressed transcript Homo sapiens 14-17 30240970-0 2018 Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin. Melatonin 111-120 H19 imprinted maternally expressed transcript Homo sapiens 52-55 30240970-2 2018 The aim of this study was to characterize the therapeutic role of melatonin as well as the underlying molecular mechanism (its effects on the expression of H19 and its downstream signaling pathways) in the treatment of PAH. Melatonin 66-75 H19 imprinted maternally expressed transcript Homo sapiens 156-159 30240970-9 2018 Finally, melatonin treatment inhibited cell proliferation; upregulated the expression of H19, miR-675-3p, and PDCD4; and downregulated the expression of miR-200a and IGF1R. Melatonin 9-18 H19 imprinted maternally expressed transcript Homo sapiens 89-92 30240970-10 2018 This study demonstrated the role of H19-miR-675-3p-IGF1R- and H19-miR-200a-PDCD4-signaling pathways in the melatonin treatment of PAH. Melatonin 107-116 H19 imprinted maternally expressed transcript Homo sapiens 36-39 30240970-10 2018 This study demonstrated the role of H19-miR-675-3p-IGF1R- and H19-miR-200a-PDCD4-signaling pathways in the melatonin treatment of PAH. Melatonin 107-116 H19 imprinted maternally expressed transcript Homo sapiens 62-65 30193235-8 2018 Results showed that prenatal exposure to NO2 was associated with higher H19 methylation in cord blood. Nitrogen Dioxide 41-44 H19 imprinted maternally expressed transcript Homo sapiens 72-75 30430771-0 2018 Long non-coding RNA H19 promotes TDRG1 expression and cisplatin resistance by sequestering miRNA-106b-5p in seminoma. Cisplatin 54-63 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30430771-5 2018 In this study, using microarray analysis, we found that long non-coding RNA H19 was upregulated while miRNA-106b-5p was downregulated in an established cisplatin-resistant TCam-2 cell line. Cisplatin 152-161 H19 imprinted maternally expressed transcript Homo sapiens 76-79 30430771-7 2018 Based on these findings, we propose that H19 promotes the expression of TDRG1 by sequestering miRNA-106b-5p and uses this mechanism to facilitate cell survival in cisplatin-based chemotherapeutic conditions. Cisplatin 163-172 H19 imprinted maternally expressed transcript Homo sapiens 41-44 30523238-6 2018 In addition, under the condition of hypoxia, the expression of transporter on cell membrane changes, and the transition of the intracellular glucose metabolism pathway from aerobic oxidation to anaerobic glycolysis is also involved in the involvement of H19. Glucose 141-148 H19 imprinted maternally expressed transcript Homo sapiens 254-257 30519041-9 2018 Results: We found that lncRNA H19 expression level manipulated breast cancer cell proliferation both in parental breast cancer cell lines and tamoxifen-resistant cell lines. Tamoxifen 142-151 H19 imprinted maternally expressed transcript Homo sapiens 30-33 30519041-10 2018 Knockdown of lncRNA H19 elevated tamoxifen sensitivity for promoting cell growth and inhibiting apoptosis in tamoxifen-resistant breast cancer cells. Tamoxifen 33-42 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30519041-10 2018 Knockdown of lncRNA H19 elevated tamoxifen sensitivity for promoting cell growth and inhibiting apoptosis in tamoxifen-resistant breast cancer cells. Tamoxifen 109-118 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30519041-11 2018 Moreover, knockdown of H19 inhibited Wnt pathway and epithelia-mesenchymal transition in tamoxifen-resistance breast cancer cells. Tamoxifen 89-98 H19 imprinted maternally expressed transcript Homo sapiens 23-26 30519041-12 2018 Conclusion: Taken together, the results of this study provided the evidence for H19 in regulating tamoxifen-resistant breast cancer and might provide novel options in the future treatment of tamoxifen-resistance breast cancer patients. Tamoxifen 98-107 H19 imprinted maternally expressed transcript Homo sapiens 80-83 30519041-12 2018 Conclusion: Taken together, the results of this study provided the evidence for H19 in regulating tamoxifen-resistant breast cancer and might provide novel options in the future treatment of tamoxifen-resistance breast cancer patients. Tamoxifen 191-200 H19 imprinted maternally expressed transcript Homo sapiens 80-83 30389909-10 2018 Notably, aspirin attenuates E2-induced cancer stem-like traits through decreasing both H19 and ERbeta expression. Aspirin 9-16 H19 imprinted maternally expressed transcript Homo sapiens 87-90 30542738-0 2018 Tumor-released lncRNA H19 promotes gefitinib resistance via packaging into exosomes in non-small cell lung cancer. Gefitinib 35-44 H19 imprinted maternally expressed transcript Homo sapiens 22-25 30542738-3 2018 To this end, the involvement and regulatory functions of lncRNA H19 wrapped by exosomes during formation of gefitinib resistance in human NSCLC were investigated. Gefitinib 108-117 H19 imprinted maternally expressed transcript Homo sapiens 64-67 30542738-5 2018 RT-qPCR assays indicated that H19 was increased in gefitinib-resistant cells when compared to sensitive parent cells. Gefitinib 51-60 H19 imprinted maternally expressed transcript Homo sapiens 30-33 30542738-6 2018 Functional experiments revealed that silencing of H19 potently promoted gefitinib-induced cell cytotoxicity. Gefitinib 72-81 H19 imprinted maternally expressed transcript Homo sapiens 50-53 30542738-8 2018 H19 wrapped in exosomes could be transferred to non-resistant cells, thus inducing gefitinib resistance. Gefitinib 83-92 H19 imprinted maternally expressed transcript Homo sapiens 0-3 30542738-9 2018 Moreover, treatment-sensitive cells with exosomes highly-expressing H19 induced gefitinib resistance, while knockdown of H19 abrogated this effect. Gefitinib 80-89 H19 imprinted maternally expressed transcript Homo sapiens 68-71 30542738-10 2018 In conclusion, H19 promoted gefitinib resistance of NSCLC cells by packaging into exosomes. Gefitinib 28-37 H19 imprinted maternally expressed transcript Homo sapiens 15-18 30451820-0 2018 Long non-coding RNA H19 confers 5-Fu resistance in colorectal cancer by promoting SIRT1-mediated autophagy. Fluorouracil 32-36 H19 imprinted maternally expressed transcript Homo sapiens 20-23 30451820-3 2018 Here, we observed lncRNA H19 was associated with the 5-Fu resistance in CRC. Fluorouracil 53-57 H19 imprinted maternally expressed transcript Homo sapiens 25-28 30451820-6 2018 Our functional studies demonstrated that H19 promoted colorectal cells 5-Fu resistance. Fluorouracil 71-75 H19 imprinted maternally expressed transcript Homo sapiens 41-44 30451820-11 2018 Our finding provides a novel mechanistic role of H19 in CRC chemoresistance, suggesting that H19 may function as a marker for prediction of chemotherapeutic response to 5-Fu. Fluorouracil 169-173 H19 imprinted maternally expressed transcript Homo sapiens 93-96 30044001-14 2018 After supernatant of keratinocytes transfected with H19 siRNAs was cocultured with PIG1 cells, the levels of MiTF, TYR and Rab27A were upregulated in PIG1 cells. Tyrosine 115-118 H19 imprinted maternally expressed transcript Homo sapiens 52-55 30096294-9 2018 Moreover, we found that in A549 cells, the treatment with A + N stimulated in p53-dependent fashion the expression of other high cooperativity p53 target genes, DRAXIN and H19. Ethanol 58-63 H19 imprinted maternally expressed transcript Homo sapiens 172-175 30096294-10 2018 Activation of antiapoptotic H19 can mechanistically explain relatively low rate of apoptosis of A549 cells exposed to A + N. Ethanol 118-123 H19 imprinted maternally expressed transcript Homo sapiens 28-31 30323617-0 2018 H19 induced by oxidative stress confers temozolomide resistance in human glioma cells via activating NF-kappaB signaling. Temozolomide 40-52 H19 imprinted maternally expressed transcript Homo sapiens 0-3 30323617-2 2018 Herein, we aimed to investigate the role of lncRNA H19 in temozolomide (TMZ) resistance of human glioma cells and the possible mechanisms. Temozolomide 58-70 H19 imprinted maternally expressed transcript Homo sapiens 51-54 30323617-2 2018 Herein, we aimed to investigate the role of lncRNA H19 in temozolomide (TMZ) resistance of human glioma cells and the possible mechanisms. Temozolomide 72-75 H19 imprinted maternally expressed transcript Homo sapiens 51-54 30323617-10 2018 Blockage of NF-kappaB activation by its inhibitor abolished TMZ resistance caused by H19 overexpression. Temozolomide 60-63 H19 imprinted maternally expressed transcript Homo sapiens 85-88 30323617-11 2018 Addition of H2O2 to induce oxidative stress largely reversed TMZ sensitivity caused by H19 knockdown. Hydrogen Peroxide 12-16 H19 imprinted maternally expressed transcript Homo sapiens 87-90 30323617-11 2018 Addition of H2O2 to induce oxidative stress largely reversed TMZ sensitivity caused by H19 knockdown. Temozolomide 61-64 H19 imprinted maternally expressed transcript Homo sapiens 87-90 29772428-0 2018 LncRNA H19 interacts with S-adenosylhomocysteine hydrolase to regulate LINE-1 Methylation in human lung-derived cells exposed to Benzo[a]pyrene. Benzo(a)pyrene 129-143 H19 imprinted maternally expressed transcript Homo sapiens 7-10 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 40-43 H19 imprinted maternally expressed transcript Homo sapiens 99-102 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 40-43 H19 imprinted maternally expressed transcript Homo sapiens 129-132 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 112-115 H19 imprinted maternally expressed transcript Homo sapiens 99-102 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 112-115 H19 imprinted maternally expressed transcript Homo sapiens 129-132 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 112-115 H19 imprinted maternally expressed transcript Homo sapiens 99-102 30190464-7 2018 Strikingly, paternally expressed genes (PEG) were largely absent from BAT and we demonstrated that H19 recruits PEG-inactivating H19-MBD1 complexes and acts as BAT-selective PEG gatekeeper. Polyethylene Glycols 112-115 H19 imprinted maternally expressed transcript Homo sapiens 129-132 29772428-3 2018 Results showed that compared to the controls, BaP-treated cells H19 expressions were increased in a dose- and time-dependent manner, whereas SAHH protein expressions were decreased. Benzo(a)pyrene 46-49 H19 imprinted maternally expressed transcript Homo sapiens 64-67 29520912-0 2018 Laser ablation synthesis of arsenic-phosphide Asm Pn clusters from As-P mixtures. arsenic-phosphide 28-45 H19 imprinted maternally expressed transcript Homo sapiens 46-49 29621481-10 2018 Levels of H19 lncRNA increased in intestinal tissues of patients with ulcerative colitis, mice with LPS-induced and polymicrobial sepsis, or mice with DSS-induced colitis, compared with controls. Dextran Sulfate 151-154 H19 imprinted maternally expressed transcript Homo sapiens 10-13 30083271-17 2018 Of note, H19 was enriched in CAF-derived conditioned medium and exosomes, which in turn promoted the stemness of CSCs and the chemoresistance of CRC cells in vitro and in vivo. cafestol palmitate 29-32 H19 imprinted maternally expressed transcript Homo sapiens 9-12 30083271-19 2018 Conclusion: CAFs promote the stemness and chemoresistance of CRC by transferring exosomal H19. cafs 12-16 H19 imprinted maternally expressed transcript Homo sapiens 90-93 30083271-21 2018 Our findings indicate that H19 expressed by CAFs of the colorectal tumor stroma contributes to tumor development and chemoresistance. cafs 44-48 H19 imprinted maternally expressed transcript Homo sapiens 27-30 29946374-7 2018 Allele-specific changes in the methylation level of H19 ICR in placental tissue (n = 26) and white blood cells (WBC, n = 8) were examined by bisulfite sequencing. hydrogen sulfite 141-150 H19 imprinted maternally expressed transcript Homo sapiens 52-55 29520849-0 2018 LncRNA H19 targets miR-22 to modulate H2 O2 -induced deregulation in nucleus pulposus cell senescence, proliferation, and ECM synthesis through Wnt signaling. Hydrogen Peroxide 38-43 H19 imprinted maternally expressed transcript Homo sapiens 7-10 29520849-4 2018 Herein, we investigated the detailed function and mechanism of H19, one of the most up-regulated lncRNAs in IDD specimens, in H2 O2 -induced cell senescence model in NPCs. Hydrogen Peroxide 126-131 H19 imprinted maternally expressed transcript Homo sapiens 63-66 29520849-5 2018 H19 could accelerate H2 O2 -induced degenerative changes by promoting cell senescence, increasing ADAMTS-5 and MMPs protein levels and Collagen I content, as well as suppressing NPC proliferation through activating Wnt/beta-catenin signaling. Hydrogen Peroxide 21-26 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29520849-7 2018 Taken together, H19 acts as a ceRNA to compete with LEF1 for miR-22, thus modulating downstream Wnt/beta-catenin signaling in NPCs; H19/miR-22/LEF1 might be a novel target for improving H2 O2 -induced NPC senescence and treatment for IDD. Hydrogen Peroxide 186-191 H19 imprinted maternally expressed transcript Homo sapiens 16-19 29520849-7 2018 Taken together, H19 acts as a ceRNA to compete with LEF1 for miR-22, thus modulating downstream Wnt/beta-catenin signaling in NPCs; H19/miR-22/LEF1 might be a novel target for improving H2 O2 -induced NPC senescence and treatment for IDD. Hydrogen Peroxide 186-191 H19 imprinted maternally expressed transcript Homo sapiens 132-135 29468525-0 2018 Valproic Acid Promotes Apoptosis and Cisplatin Sensitivity Through Downregulation of H19 Noncoding RNA in Ovarian A2780 Cells. Valproic Acid 0-13 H19 imprinted maternally expressed transcript Homo sapiens 85-88 29468525-2 2018 H19 is a lncRNA involving in cisplatin resistance in cancers. Cisplatin 29-38 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29468525-9 2018 Our results demonstrate that H19 knockdown by siRNA induced apoptosis and sensitized the A2780/CP cells to cisplatin-induced cytotoxicity. Cisplatin 107-116 H19 imprinted maternally expressed transcript Homo sapiens 29-32 29468525-10 2018 These data indicated that VPA negatively regulates the expression of H19 in ovarian cancer cells, which subsequently leads to apoptosis induction, cell proliferation inhibition, and overwhelming to cisplatin resistance. Cisplatin 198-207 H19 imprinted maternally expressed transcript Homo sapiens 69-72 29468525-11 2018 The implication of H19 EZH2 p21/PTEN pathway by VPA treatment suggests that we could repurpose an old drug, valproic acid, as an effective drug for treatment of ovarian cancer in the future. Valproic Acid 108-121 H19 imprinted maternally expressed transcript Homo sapiens 19-22 30064499-11 2018 Correlations of ASMMDXA with ASMM estimated by the models were as follows: ASM1, r = 0.68, R2 = 0.46, SEE = 2.02 kg; ASM2, r = 0.90, R2 = 0.81, SEE = 1.18 kg; ASM3, r = 0.90, R2 = 0.81, SEE = 1.17 kg; and ASM4, r = 0.91, R2 = 0.82, SEE = 1.14 kg. asmmdxa 16-23 H19 imprinted maternally expressed transcript Homo sapiens 75-79 30064499-11 2018 Correlations of ASMMDXA with ASMM estimated by the models were as follows: ASM1, r = 0.68, R2 = 0.46, SEE = 2.02 kg; ASM2, r = 0.90, R2 = 0.81, SEE = 1.18 kg; ASM3, r = 0.90, R2 = 0.81, SEE = 1.17 kg; and ASM4, r = 0.91, R2 = 0.82, SEE = 1.14 kg. asmm 16-20 H19 imprinted maternally expressed transcript Homo sapiens 75-79 29411215-3 2018 In the present study, we found that the expression of H19 was significantly increased in transforming growth factor-beta (TGF-beta)-induced fibroblast proliferation and bleomycin-(BLM) induced lung fibrosis (p < 0.05). Bleomycin 169-178 H19 imprinted maternally expressed transcript Homo sapiens 54-57 29520912-0 2018 Laser ablation synthesis of arsenic-phosphide Asm Pn clusters from As-P mixtures. Aspartic Acid 67-71 H19 imprinted maternally expressed transcript Homo sapiens 46-49 29344674-12 2018 In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. mir-138 119-126 H19 imprinted maternally expressed transcript Homo sapiens 13-16 29703210-11 2018 RESULTS: We showed both in retinoid-treated cell lines and in APL patient cells an inverse relationship between the expression of H19 and the expression and activity of hTERT. Retinoids 27-35 H19 imprinted maternally expressed transcript Homo sapiens 130-133 29698523-0 2018 Urine mercury levels correlate with DNA methylation of imprinting gene H19 in the sperm of reproductive-aged men. Mercury 6-13 H19 imprinted maternally expressed transcript Homo sapiens 71-74 29698523-16 2018 CONCLUSIONS: Mercury non-occupational environmental exposure in reproductive-aged men was associated with altered DNA methylation outcomes at imprinting gene H19 in sperm, implicating the susceptibility of the developing sperm for environmental insults. Mercury 13-20 H19 imprinted maternally expressed transcript Homo sapiens 158-161 29643943-11 2018 In the follow-up of patients, H19 expression in CR phase was lower than diagnosis time and returned at relapse time. Chromium 48-50 H19 imprinted maternally expressed transcript Homo sapiens 30-33 29140550-4 2018 H19 and PTBP1 are up-regulated by fatty acids in hepatocytes and in diet-induced fatty liver, which further augments lipid accumulation. Fatty Acids 34-45 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29140550-6 2018 Deletion of H19 or knockdown of PTBP1 abolishes high-fat and high-sucrose diet-induced steatosis. Sucrose 66-73 H19 imprinted maternally expressed transcript Homo sapiens 12-15 29253550-0 2018 Long non-coding RNA H19 mediates mechanical tension-induced osteogenesis of bone marrow mesenchymal stem cells via FAK by sponging miR-138. mir-138 131-138 H19 imprinted maternally expressed transcript Homo sapiens 20-23 29344674-12 2018 In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. mir-138 119-126 H19 imprinted maternally expressed transcript Homo sapiens 191-194 29344674-12 2018 In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. mir-138 146-153 H19 imprinted maternally expressed transcript Homo sapiens 13-16 29344674-12 2018 In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. mir-138 146-153 H19 imprinted maternally expressed transcript Homo sapiens 191-194 29415742-11 2018 Moreover, miR-148b inhibitor could reverse the effects of H19 depletion on proliferation and apoptosis in ox-LDL-stimulated HA-VSMCs. ha-vsmcs 124-132 H19 imprinted maternally expressed transcript Homo sapiens 58-61 29344674-13 2018 On the whole, our findings suggest that H19 functions as an oncogene by inhibiting miR-138 and facilitating EZH2 expression in OSCC. mir-138 83-90 H19 imprinted maternally expressed transcript Homo sapiens 40-43 31938202-5 2018 RESULTS: The optical density value of A375/H19+ cells increased after incubation with MTT reagent for 12 h (P < 0.05), and the transwell assay showed that the average penetration rate of A375/H19+ cells significantly increased (P < 0.001). thiazolyl blue 86-89 H19 imprinted maternally expressed transcript Homo sapiens 43-46 31938202-5 2018 RESULTS: The optical density value of A375/H19+ cells increased after incubation with MTT reagent for 12 h (P < 0.05), and the transwell assay showed that the average penetration rate of A375/H19+ cells significantly increased (P < 0.001). thiazolyl blue 86-89 H19 imprinted maternally expressed transcript Homo sapiens 195-198 29391808-0 2018 The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/beta-Catenin pathway. Temozolomide 79-91 H19 imprinted maternally expressed transcript Homo sapiens 24-27 29431097-4 2018 The tunicate Ciona emerged as an attractive model to study early cardiopharyngeal development at high resolution: through two asymmetric and oriented divisions, defined cardiopharyngeal progenitors produce distinct first and second heart precursors, and pharyngeal muscle (aka atrial siphon muscle, ASM) precursors. tunicate ciona 4-18 H19 imprinted maternally expressed transcript Homo sapiens 299-302 29391808-6 2018 Knockdown of H19 expression using specific shRNA in U-251TMZ and M059JTMZ led to decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis rates, indicating that the silencing of H19 decreased chemoresistance of glioma cells to TMZ. Temozolomide 57-60 H19 imprinted maternally expressed transcript Homo sapiens 13-16 29391808-6 2018 Knockdown of H19 expression using specific shRNA in U-251TMZ and M059JTMZ led to decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis rates, indicating that the silencing of H19 decreased chemoresistance of glioma cells to TMZ. Temozolomide 70-73 H19 imprinted maternally expressed transcript Homo sapiens 13-16 29391808-11 2018 Conclusion: Taken together, our data suggest that H19 decreased chemoresistance of glioma cells to TMZ by suppressing EMT via the inhibition of Wnt/beta-Catenin pathway. Temozolomide 99-102 H19 imprinted maternally expressed transcript Homo sapiens 50-53 30497079-8 2018 RESULTS: Here we report that treating ETR cells with Tam or Fulvestrant increases H19 expression and that it"s decreased expression overcomes resistance to Tam and Fulvestrant in these cells. Tamoxifen 53-56 H19 imprinted maternally expressed transcript Homo sapiens 82-85 29954239-7 2018 Moreover, Let-7 controlled Wnt signaling pathway activity could be strengthened due to the miR146 inhibition of H19, later of which was often activated in stem cells group with functional existence of Wnt signaling. mir146 91-97 H19 imprinted maternally expressed transcript Homo sapiens 112-115 30497079-8 2018 RESULTS: Here we report that treating ETR cells with Tam or Fulvestrant increases H19 expression and that it"s decreased expression overcomes resistance to Tam and Fulvestrant in these cells. Fulvestrant 60-71 H19 imprinted maternally expressed transcript Homo sapiens 82-85 30497079-9 2018 Interestingly, H19 expression is regulated by Notch and HGF signaling in the ETR cells and pharmacological inhibitors of Notch and c-MET signaling together significantly reverse resistance to Tam and Fulvestrant in an H19-dependent manner in these cells. Tamoxifen 192-195 H19 imprinted maternally expressed transcript Homo sapiens 15-18 29121487-5 2018 We stratified by LQTS genotype and predominant mechanism of ASM action (Na+ channel blocker and gamma-aminobutyric acid modifier.) gamma-Aminobutyric Acid 96-119 H19 imprinted maternally expressed transcript Homo sapiens 60-63 28708434-8 2017 Peak calcium release in response to histamine was diminished, and depended on the synthesis of cyclo-oxygenase-1 products by ASM and on prostaglandin E receptors 2 and 4. Calcium 5-12 H19 imprinted maternally expressed transcript Homo sapiens 125-128 29258985-4 2017 On the other hand, H19 also modulates the target genes in trans, including sponging let-7, miR-106 or miR-29 to mediate myocyte glucose uptake, cardiomyocyte proliferation and tendon repair, as well as promote embryonic development and muscle regeneration through binding to MBD1 as a chromatin modifier. Glucose 128-135 H19 imprinted maternally expressed transcript Homo sapiens 19-22 29215608-0 2017 H19 lncRNA alters methylation and expression of Hnf4alpha in the liver of metformin-exposed fetuses. Metformin 74-83 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29215608-7 2017 We also provide evidence that altered H19 expression is a direct effect of metformin in the fetal liver. Metformin 75-84 H19 imprinted maternally expressed transcript Homo sapiens 38-41 29215608-8 2017 Our results suggest that metformin from the mother can directly act upon the fetal liver to modify Hnf4alpha expression, a key factor for both liver development and function, and that perturbation of this H19/Hnf4alpha-mediated pathway may contribute to the fetal origin of adult metabolic abnormalities. Metformin 25-34 H19 imprinted maternally expressed transcript Homo sapiens 205-208 28708434-8 2017 Peak calcium release in response to histamine was diminished, and depended on the synthesis of cyclo-oxygenase-1 products by ASM and on prostaglandin E receptors 2 and 4. Histamine 36-45 H19 imprinted maternally expressed transcript Homo sapiens 125-128 28778973-0 2017 Impact of folic acid intake during pregnancy on genomic imprinting of IGF2/H19 and 1-carbon metabolism. Folic Acid 10-20 H19 imprinted maternally expressed transcript Homo sapiens 75-84 28295500-5 2017 The existing evidence along with the absence of relevant data in south of Iran prompted us to study the methylation of H19 imprinted gene in spermatozoa of idiopathic infertile patients (males with abnormalities in sperm parameters) and healthy controls by Combined Bisulfite Restriction Analysis. hydrogen sulfite 266-275 H19 imprinted maternally expressed transcript Homo sapiens 119-122 28778973-0 2017 Impact of folic acid intake during pregnancy on genomic imprinting of IGF2/H19 and 1-carbon metabolism. Carbon 85-91 H19 imprinted maternally expressed transcript Homo sapiens 75-84 28778973-3 2017 We investigated the association between folic acid supplementation during pregnancy and loss of imprinting (LOI) of IGF2 and H19 genes in placentas and cord blood of 90 mother-child dyads in association with the methylenetetrahydrofolate reductase (MTHFR) genotype. Folic Acid 40-50 H19 imprinted maternally expressed transcript Homo sapiens 125-128 28778973-10 2017 Impact of folic acid intake during pregnancy on genomic imprinting of IGF2/H19 and 1-carbon metabolism. Folic Acid 10-20 H19 imprinted maternally expressed transcript Homo sapiens 75-84 28778973-10 2017 Impact of folic acid intake during pregnancy on genomic imprinting of IGF2/H19 and 1-carbon metabolism. Carbon 85-91 H19 imprinted maternally expressed transcript Homo sapiens 75-84 30895230-0 2017 rs10732516 polymorphism at the IGF2/H19 locus associates with a genotype-specific trend in placental DNA methylation and head circumference of prenatally alcohol-exposed newborns. Alcohols 154-161 H19 imprinted maternally expressed transcript Homo sapiens 36-39 30895230-1 2017 Study Question: Does prenatal alcohol exposure (PAE) affect regulation of the insulin-like growth factor 2 (IGF2)/H19 locus in placenta and the growth-restricted phenotype of newborns? Alcohols 30-37 H19 imprinted maternally expressed transcript Homo sapiens 114-117 30895230-7 2017 Study Design Size Duration: By grouping 39 alcohol-exposed and 100 control samples according to rs10732516 polymorphism we explored alcohol-induced, genotype-specific changes in DNA methylation at the H19 ICR and the promoter region of H19 (H19 differentially methylated region). Alcohols 132-139 H19 imprinted maternally expressed transcript Homo sapiens 201-204 30895230-7 2017 Study Design Size Duration: By grouping 39 alcohol-exposed and 100 control samples according to rs10732516 polymorphism we explored alcohol-induced, genotype-specific changes in DNA methylation at the H19 ICR and the promoter region of H19 (H19 differentially methylated region). Alcohols 132-139 H19 imprinted maternally expressed transcript Homo sapiens 236-239 30895230-7 2017 Study Design Size Duration: By grouping 39 alcohol-exposed and 100 control samples according to rs10732516 polymorphism we explored alcohol-induced, genotype-specific changes in DNA methylation at the H19 ICR and the promoter region of H19 (H19 differentially methylated region). Alcohols 132-139 H19 imprinted maternally expressed transcript Homo sapiens 236-239 28867213-0 2017 Transgenerational pancreatic impairment with Igf2/H19 epigenetic alteration induced by p,p"-DDE exposure in early life. Dichlorodiphenyl Dichloroethylene 87-95 H19 imprinted maternally expressed transcript Homo sapiens 50-53 30895230-11 2017 Main Results and the Role of Chance: We observed a consistent trend in genotype-specific changes in DNA methylation at H19 ICR in alcohol-exposed placentas. Alcohols 130-137 H19 imprinted maternally expressed transcript Homo sapiens 119-122 28867213-8 2017 Results indicated that F1 offspring in p,p"-DDE group exhibited impaired glucose tolerance (IGT), abnormal insulin secretion, beta-cell dysfunction and altered Igf2 and H19 expression induced by Igf2/H19 hypomethylation, which could be transferred to the F3 offspring through the male germ line. Dichlorodiphenyl Dichloroethylene 44-47 H19 imprinted maternally expressed transcript Homo sapiens 169-172 30895230-13 2017 In addition to decreased IGF2 mRNA expression in alcohol-exposed placentas of this specific genotype (P = 0.03), we observed significantly increased expression of H19 in relation to IGF2 when comparing all alcohol-exposed placentas to unexposed controls (P = 0.006). Alcohols 206-213 H19 imprinted maternally expressed transcript Homo sapiens 163-166 28867213-8 2017 Results indicated that F1 offspring in p,p"-DDE group exhibited impaired glucose tolerance (IGT), abnormal insulin secretion, beta-cell dysfunction and altered Igf2 and H19 expression induced by Igf2/H19 hypomethylation, which could be transferred to the F3 offspring through the male germ line. Dichlorodiphenyl Dichloroethylene 44-47 H19 imprinted maternally expressed transcript Homo sapiens 200-203 29190892-0 2017 LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway. Doxorubicin 34-45 H19 imprinted maternally expressed transcript Homo sapiens 7-10 29076348-1 2017 AIM: ASM, which hydrolyzes sphingomyelin into ceramide, is recognized as a therapeutic target for UV-induced skin damage. Sphingomyelins 27-40 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29076348-1 2017 AIM: ASM, which hydrolyzes sphingomyelin into ceramide, is recognized as a therapeutic target for UV-induced skin damage. Ceramides 46-54 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29076348-3 2017 Here we synthesized several series of 1,3,6,7-tetrahydroxy-xanthone derivatives as novel ASM inhibitors. 1,3,6,7-tetrahydroxyxanthone 38-67 H19 imprinted maternally expressed transcript Homo sapiens 89-92 29190892-3 2017 In the present study, we investigated the role and molecular mechanism of H19 lncRNA in chemoresistance development by using doxorubicin (Dox) resistance in breast cancer cells as a model system. Doxorubicin 125-136 H19 imprinted maternally expressed transcript Homo sapiens 74-77 29190892-3 2017 In the present study, we investigated the role and molecular mechanism of H19 lncRNA in chemoresistance development by using doxorubicin (Dox) resistance in breast cancer cells as a model system. Doxorubicin 138-141 H19 imprinted maternally expressed transcript Homo sapiens 74-77 29190892-4 2017 H19 lncRNA expression was significantly increased in anthracycline-treated and Dox-resistant MCF-7 breast cancer cells. Anthracyclines 53-66 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29190892-4 2017 H19 lncRNA expression was significantly increased in anthracycline-treated and Dox-resistant MCF-7 breast cancer cells. Doxorubicin 79-82 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 69-83 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 69-83 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 69-83 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 88-98 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 88-98 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 88-98 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 220-234 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 220-234 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Anthracyclines 220-234 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 239-249 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 239-249 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Paclitaxel 239-249 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-6 2017 Furthermore, gene expression profiling analysis revealed that a total of 192 genes were associated with H19-mediated Dox resistance. Doxorubicin 117-120 H19 imprinted maternally expressed transcript Homo sapiens 104-107 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 119-122 H19 imprinted maternally expressed transcript Homo sapiens 105-108 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 119-122 H19 imprinted maternally expressed transcript Homo sapiens 262-265 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 210-213 H19 imprinted maternally expressed transcript Homo sapiens 105-108 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 210-213 H19 imprinted maternally expressed transcript Homo sapiens 262-265 28865728-0 2017 Gender-specific association of exposure to non-dioxin-like polychlorinated biphenyls during pregnancy with methylation levels of H19 and long interspersed nuclear element-1 in cord blood in the Hokkaido study. Dioxins 47-53 H19 imprinted maternally expressed transcript Homo sapiens 129-172 31225433-6 2017 Clonogenicity and proliferation assays showed that H19 overexpression could suppress tumor cell survival and proliferation after treatment with either sorafenib or doxorubicin, suggesting chemosensitizing actions of H19. Sorafenib 151-160 H19 imprinted maternally expressed transcript Homo sapiens 51-54 31225433-6 2017 Clonogenicity and proliferation assays showed that H19 overexpression could suppress tumor cell survival and proliferation after treatment with either sorafenib or doxorubicin, suggesting chemosensitizing actions of H19. Doxorubicin 164-175 H19 imprinted maternally expressed transcript Homo sapiens 51-54 31225433-10 2017 Chemoresistant cells were sensitized after H19 overexpression by either increasing the cytotoxic action of doxorubicin or decreasing cell proliferation upon sorafenib treatment. Doxorubicin 107-118 H19 imprinted maternally expressed transcript Homo sapiens 43-46 31225433-10 2017 Chemoresistant cells were sensitized after H19 overexpression by either increasing the cytotoxic action of doxorubicin or decreasing cell proliferation upon sorafenib treatment. Sorafenib 157-166 H19 imprinted maternally expressed transcript Homo sapiens 43-46 28865728-0 2017 Gender-specific association of exposure to non-dioxin-like polychlorinated biphenyls during pregnancy with methylation levels of H19 and long interspersed nuclear element-1 in cord blood in the Hokkaido study. Polychlorinated Biphenyls 59-84 H19 imprinted maternally expressed transcript Homo sapiens 129-172 28865728-2 2017 To date, however, studies on the associations between prenatal exposure to PCBs and alterations in methylation of IGF-2, H19, and LINE-1 are lacking. Polychlorinated Biphenyls 75-79 H19 imprinted maternally expressed transcript Homo sapiens 121-124 28865728-7 2017 RESULTS: We observed a 0.017 (95% confidence interval [CI]: 0.003-0.031) increase in the log10-transformed H19 methylation levels (%) in cord blood for each ten-fold increase in the levels of decachlorinated biphenyls (decaCBs) in maternal blood among all infants. decachlorinated biphenyls 192-217 H19 imprinted maternally expressed transcript Homo sapiens 107-110 28865728-7 2017 RESULTS: We observed a 0.017 (95% confidence interval [CI]: 0.003-0.031) increase in the log10-transformed H19 methylation levels (%) in cord blood for each ten-fold increase in the levels of decachlorinated biphenyls (decaCBs) in maternal blood among all infants. decacbs 219-226 H19 imprinted maternally expressed transcript Homo sapiens 107-110 28865728-9 2017 In particular, we observed a dose-dependent association of the decaCB levels in maternal blood with the H19 methylation levels among female infants (P value for trend=0.040); likewise a dose-dependent association of heptaCB levels was observed with LINE-1 methylation levels among female infants (P value for trend=0.015). decacb 63-69 H19 imprinted maternally expressed transcript Homo sapiens 104-107 28865728-11 2017 CONCLUSION: Our results suggest that the dose-dependent association between prenatal exposure to specific non-dioxin-like PCBs and increases in the H19 and LINE-1 methylation levels in cord blood might be more predominant in females than in males. Dioxins 110-116 H19 imprinted maternally expressed transcript Homo sapiens 148-151 28865728-11 2017 CONCLUSION: Our results suggest that the dose-dependent association between prenatal exposure to specific non-dioxin-like PCBs and increases in the H19 and LINE-1 methylation levels in cord blood might be more predominant in females than in males. Polychlorinated Biphenyls 122-126 H19 imprinted maternally expressed transcript Homo sapiens 148-151 27553991-0 2017 Effects of prenatal perfluoroalkyl acid exposure on cord blood IGF2/H19 methylation and ponderal index: The Hokkaido Study. perfluoroalkyl acid 20-39 H19 imprinted maternally expressed transcript Homo sapiens 68-71 28328238-0 2017 Valproic Acid Induces Decreased Expression of H19 Promoting Cell Apoptosis in A549 Cells. Valproic Acid 0-13 H19 imprinted maternally expressed transcript Homo sapiens 46-49 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Valproic Acid 118-131 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Valproic Acid 133-136 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Ascorbic Acid 139-152 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Vinyl Chloride 154-156 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Azacitidine 163-177 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28328238-2 2017 In the present study, we attempted to treat the abnormal expression and methylation status of H19 in A549 cells using valproic acid (VPA), ascorbic acid (Vc), and 5-aza-Cytidine (5-Aza). Azacitidine 179-184 H19 imprinted maternally expressed transcript Homo sapiens 94-97 28358427-4 2017 Besides, miR-138 was predicted a target of H19, and low expression of miR-138 was found in colon cancer tissues and cells. mir-138 9-16 H19 imprinted maternally expressed transcript Homo sapiens 43-46 28358427-4 2017 Besides, miR-138 was predicted a target of H19, and low expression of miR-138 was found in colon cancer tissues and cells. mir-138 70-77 H19 imprinted maternally expressed transcript Homo sapiens 43-46 28358427-5 2017 The silence of H19 strongly increased the expression of miR-138. mir-138 56-63 H19 imprinted maternally expressed transcript Homo sapiens 15-18 28358427-6 2017 The decreased level of miR-138 was elevated adding miR-138 mimic in RKO cells transfected with lncRNA-H19. mir-138 23-30 H19 imprinted maternally expressed transcript Homo sapiens 102-105 28358427-6 2017 The decreased level of miR-138 was elevated adding miR-138 mimic in RKO cells transfected with lncRNA-H19. mir-138 51-58 H19 imprinted maternally expressed transcript Homo sapiens 102-105 28358427-7 2017 Similarly, the upregulated level of miR-138 was downregulated adding miR-138 inhibitor in RKO cells transfected with H19 shRNA. mir-138 36-43 H19 imprinted maternally expressed transcript Homo sapiens 117-120 28358427-7 2017 Similarly, the upregulated level of miR-138 was downregulated adding miR-138 inhibitor in RKO cells transfected with H19 shRNA. mir-138 69-76 H19 imprinted maternally expressed transcript Homo sapiens 117-120 28358427-8 2017 The luciferase reporter confirmed the targeting reaction between H19 and miR-138. mir-138 73-80 H19 imprinted maternally expressed transcript Homo sapiens 65-68 28154921-0 2017 A phase 1/2a, dose-escalation, safety, pharmacokinetic, and preliminary efficacy study of intraperitoneal administration of BC-819 (H19-DTA) in subjects with recurrent ovarian/peritoneal cancer. bc-819 124-130 H19 imprinted maternally expressed transcript Homo sapiens 132-135 29492305-10 2017 Exposure to triphenyl phosphate was associated with hypermethylation at the GRB10 DMR; and tris(1,3-dichloro-2-propyl) phosphate exposure was associated with altered methylation at the MEG3 and H19 DMRs. tris(1,3-dichloro-2-propyl)phosphate 91-128 H19 imprinted maternally expressed transcript Homo sapiens 194-197 28933364-4 2017 H19 participates in the epigenetic regulation of many processes impacting diseases, such as activating the miR-200 pathway by histone acetylation to inhibit the epithelial-mesenchymal transition to suppress tumor metastasis. mir-200 107-114 H19 imprinted maternally expressed transcript Homo sapiens 0-3 28318372-7 2017 ASM/Ht2 were positively associated with vitamin D levels, but negatively associated with white blood cell counts and HOMA-IR by multiple regression analysis. Vitamin D 40-49 H19 imprinted maternally expressed transcript Homo sapiens 0-3 27775072-4 2017 Metformin acts by upregulating microRNA let-7 through AMPK activation, leading to degradation of H19 long noncoding RNA, which normally binds to and inactivates SAHH. Metformin 0-9 H19 imprinted maternally expressed transcript Homo sapiens 97-100 27775072-6 2017 This metformin-induced H19 repression and alteration of gene methylation are recapitulated in endometrial cancer tissue samples obtained from patients treated with antidiabetic doses of metformin. Metformin 5-14 H19 imprinted maternally expressed transcript Homo sapiens 23-26 27775072-6 2017 This metformin-induced H19 repression and alteration of gene methylation are recapitulated in endometrial cancer tissue samples obtained from patients treated with antidiabetic doses of metformin. Metformin 186-195 H19 imprinted maternally expressed transcript Homo sapiens 23-26 28189050-0 2017 H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells. Calcitriol 41-52 H19 imprinted maternally expressed transcript Homo sapiens 0-3 28189050-8 2017 Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo. Calcitriol 73-84 H19 imprinted maternally expressed transcript Homo sapiens 13-16 28189050-9 2017 Together, these results suggested that H19 overexpression might be one of the mechanisms underlying the development of resistance to the treatment with 1,25(OH)2D3 in the advanced stage of colon cancer. Calcitriol 152-163 H19 imprinted maternally expressed transcript Homo sapiens 39-42 28193296-8 2017 In both men and women, ASM/Wt was negatively correlated with higher triglycerides (TG) and positively correlated with serum high-density lipoprotein cholesterol (HDL-C), but these associations were not found in height-adjusted ASM. Triglycerides 68-81 H19 imprinted maternally expressed transcript Homo sapiens 23-26 28203482-10 2017 Autophagy inducer, rapamycin, abolished lncRNA H19 effect. Sirolimus 19-28 H19 imprinted maternally expressed transcript Homo sapiens 47-50 29658248-6 2017 After transfection of H19 siRNA, the expressions of H19 were remarkably decreased in the DU145 and PC 3 prostate cancer cells in comparison with those in the blank control and negative control groups (P< 0.01), and so were the proliferation of and the glucose and lactate levels in the DU145 and PC 3 cells (P< 0.01). Glucose 255-262 H19 imprinted maternally expressed transcript Homo sapiens 22-25 29658248-6 2017 After transfection of H19 siRNA, the expressions of H19 were remarkably decreased in the DU145 and PC 3 prostate cancer cells in comparison with those in the blank control and negative control groups (P< 0.01), and so were the proliferation of and the glucose and lactate levels in the DU145 and PC 3 cells (P< 0.01). Glucose 255-262 H19 imprinted maternally expressed transcript Homo sapiens 52-55 29658248-6 2017 After transfection of H19 siRNA, the expressions of H19 were remarkably decreased in the DU145 and PC 3 prostate cancer cells in comparison with those in the blank control and negative control groups (P< 0.01), and so were the proliferation of and the glucose and lactate levels in the DU145 and PC 3 cells (P< 0.01). Lactic Acid 267-274 H19 imprinted maternally expressed transcript Homo sapiens 22-25 29658248-6 2017 After transfection of H19 siRNA, the expressions of H19 were remarkably decreased in the DU145 and PC 3 prostate cancer cells in comparison with those in the blank control and negative control groups (P< 0.01), and so were the proliferation of and the glucose and lactate levels in the DU145 and PC 3 cells (P< 0.01). Lactic Acid 267-274 H19 imprinted maternally expressed transcript Homo sapiens 52-55 27919747-0 2017 H19 mediates methotrexate resistance in colorectal cancer through activating Wnt/beta-catenin pathway. Methotrexate 13-25 H19 imprinted maternally expressed transcript Homo sapiens 0-3 27919747-9 2017 Further investigation showed that H19 knockdown sensitized the MTX resistance in HT-29-R cells while its overexpression improved the MTX resistance in the parental cells, suggesting that H19 mediate MTX resistance. Methotrexate 63-66 H19 imprinted maternally expressed transcript Homo sapiens 34-37 27919747-11 2017 In conclusion, H19 mediated MTX resistance via activating Wnt/beta-catenin signaling, which help to develop H19 as a promising therapeutic target for MTX resistant CRC. Methotrexate 28-31 H19 imprinted maternally expressed transcript Homo sapiens 15-18 27919747-11 2017 In conclusion, H19 mediated MTX resistance via activating Wnt/beta-catenin signaling, which help to develop H19 as a promising therapeutic target for MTX resistant CRC. Methotrexate 28-31 H19 imprinted maternally expressed transcript Homo sapiens 108-111 27919747-11 2017 In conclusion, H19 mediated MTX resistance via activating Wnt/beta-catenin signaling, which help to develop H19 as a promising therapeutic target for MTX resistant CRC. Methotrexate 150-153 H19 imprinted maternally expressed transcript Homo sapiens 15-18 27919747-11 2017 In conclusion, H19 mediated MTX resistance via activating Wnt/beta-catenin signaling, which help to develop H19 as a promising therapeutic target for MTX resistant CRC. Methotrexate 150-153 H19 imprinted maternally expressed transcript Homo sapiens 108-111 27911863-0 2017 Correlation of long non-coding RNA H19 expression with cisplatin-resistance and clinical outcome in lung adenocarcinoma. Cisplatin 55-64 H19 imprinted maternally expressed transcript Homo sapiens 35-38 27911863-2 2017 The present study aimed to investigate the correlation of long non-coding RNA (lncRNA) H19 with cisplatin-resistance and clinical outcome in lung adenocarcinoma. Cisplatin 96-105 H19 imprinted maternally expressed transcript Homo sapiens 87-90 27911863-3 2017 In our study, the expression of H19 in cisplatin-resistant A549/DDP cells was unregulated. Cisplatin 39-48 H19 imprinted maternally expressed transcript Homo sapiens 32-35 27911863-4 2017 Knockdown of H19 restored the response of A549/DDP cells to cisplatin. Cisplatin 60-69 H19 imprinted maternally expressed transcript Homo sapiens 13-16 27911863-7 2017 Overexpression of H19 was negatively correlated with cisplatin-based chemotherapy response in patients. Cisplatin 53-62 H19 imprinted maternally expressed transcript Homo sapiens 18-21 27911863-9 2017 In summary, H19-mediated regulation of cisplatin resistance in human lung adenocarcinoma cells is demonstrated for the first time. Cisplatin 39-48 H19 imprinted maternally expressed transcript Homo sapiens 12-15 28105222-10 2016 Furthermore, while curcumin induced cell apoptosis and enhanced the expression ratio of Bax/Bcl-2, which are downstream molecules of p53, ectopic expression of H19 inhibited curcumin-induced cell apoptosis. Curcumin 19-27 H19 imprinted maternally expressed transcript Homo sapiens 160-163 27845892-5 2016 In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. Paclitaxel 108-118 H19 imprinted maternally expressed transcript Homo sapiens 52-55 27845892-5 2016 In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERalpha-positive breast cancer cells, but not in ERalpha-negative breast cancer cells. Paclitaxel 120-123 H19 imprinted maternally expressed transcript Homo sapiens 52-55 27845892-6 2016 LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. Paclitaxel 52-55 H19 imprinted maternally expressed transcript Homo sapiens 7-10 27845892-7 2016 H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Lysine 126-132 H19 imprinted maternally expressed transcript Homo sapiens 0-3 28105222-0 2016 Curcumin suppresses the proliferation of gastric cancer cells by downregulating H19. Curcumin 0-8 H19 imprinted maternally expressed transcript Homo sapiens 80-83 28105222-10 2016 Furthermore, while curcumin induced cell apoptosis and enhanced the expression ratio of Bax/Bcl-2, which are downstream molecules of p53, ectopic expression of H19 inhibited curcumin-induced cell apoptosis. Curcumin 174-182 H19 imprinted maternally expressed transcript Homo sapiens 160-163 28105222-3 2016 The aim of this study was to assess the role of H19 in curcumin-induced proliferative inhibition of gastric cancer. Curcumin 55-63 H19 imprinted maternally expressed transcript Homo sapiens 48-51 28105222-11 2016 In addition, curcumin decreased the expression of the c-Myc oncogene, and exogenous c-Myc protein reversed the curcumin-induced downregulation of H19 expression. Curcumin 111-119 H19 imprinted maternally expressed transcript Homo sapiens 146-149 28105222-8 2016 The present study demonstrated that curcumin inhibited the proliferation of SGC7901 cells and suppressed H19 expression in a concentration-dependent manner, while p53 expression was enhanced. Curcumin 36-44 H19 imprinted maternally expressed transcript Homo sapiens 105-108 28105222-9 2016 Ectopic expression of H19 in SGC7901 cells reversed curcumin-induced proliferative inhibition and downregulated p53 expression. Curcumin 52-60 H19 imprinted maternally expressed transcript Homo sapiens 22-25 28105222-12 2016 These results suggested that curcumin inhibits the proliferation of gastric cancer cells by downregulating the c-Myc/H19 pathway. Curcumin 29-37 H19 imprinted maternally expressed transcript Homo sapiens 117-120 27698867-5 2016 H19 siRNA treatment markedly inhibited the proliferation of keloid fibroblasts, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (P=0.008). thiazolyl blue 95-155 H19 imprinted maternally expressed transcript Homo sapiens 0-3 27662231-2 2016 Three NMR structures (glycocin F, ASM1 and sublancin 168), two with helix-loop-helix Cs alpha/alpha folds, are deposited in the PDB. Cesium 85-87 H19 imprinted maternally expressed transcript Homo sapiens 34-38 27809873-7 2016 We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. Hydrogen Peroxide 235-239 H19 imprinted maternally expressed transcript Homo sapiens 32-35 26983719-6 2016 H19 knocked down GBM cells also displayed decreased cellular proliferation and a higher apoptosis rate when induced by temozolomide. Temozolomide 119-131 H19 imprinted maternally expressed transcript Homo sapiens 0-3 27062045-0 2016 Long noncoding RNA H19 mediates melatonin inhibition of premature senescence of c-kit(+) cardiac progenitor cells by promoting miR-675. Melatonin 32-41 H19 imprinted maternally expressed transcript Homo sapiens 19-22 27687660-5 2016 CONCLUSION: Propofol-induced cell migration and invasion suppression are partially mediated by down-regulating H19 in MDA-MB-231 cells in vitro. Propofol 12-20 H19 imprinted maternally expressed transcript Homo sapiens 111-114 27368064-10 2016 In the non-sarcopenia population, ASM/HT(2) presents as renal function risk factor, which perhaps associated with higher muscle mass to induce a greater underestimation for creatinine and urinary albumin. Creatinine 173-183 H19 imprinted maternally expressed transcript Homo sapiens 34-37 27687660-0 2016 [Propofol suppresses migration and invasion of breast cancer MDA-MB-231 cells by down-regulating H19]. Propofol 1-9 H19 imprinted maternally expressed transcript Homo sapiens 97-100 27687660-1 2016 OBJECTIVE: To explore the effect of propofol on H19 expression, migration and invasion of human breast cancer MDA-MB-231 cells in vitro. Propofol 36-44 H19 imprinted maternally expressed transcript Homo sapiens 48-51 27062045-8 2016 Interestingly, we found that long noncoding RNA H19 and its derived miR-675 were downregulated by H2 O2 in CPCs, but melatonin treatment could counter this alteration. Hydrogen Peroxide 98-103 H19 imprinted maternally expressed transcript Homo sapiens 48-51 27062045-8 2016 Interestingly, we found that long noncoding RNA H19 and its derived miR-675 were downregulated by H2 O2 in CPCs, but melatonin treatment could counter this alteration. cpcs 107-111 H19 imprinted maternally expressed transcript Homo sapiens 48-51 27062045-8 2016 Interestingly, we found that long noncoding RNA H19 and its derived miR-675 were downregulated by H2 O2 in CPCs, but melatonin treatment could counter this alteration. Melatonin 117-126 H19 imprinted maternally expressed transcript Homo sapiens 48-51 27062045-9 2016 Furthermore, knockdown of H19 or miR-675 blocked antisenescence actions of melatonin on H2 O2 -treated CPCs. Melatonin 75-84 H19 imprinted maternally expressed transcript Homo sapiens 26-29 27062045-9 2016 Furthermore, knockdown of H19 or miR-675 blocked antisenescence actions of melatonin on H2 O2 -treated CPCs. Hydrogen Peroxide 88-93 H19 imprinted maternally expressed transcript Homo sapiens 26-29 27062045-9 2016 Furthermore, knockdown of H19 or miR-675 blocked antisenescence actions of melatonin on H2 O2 -treated CPCs. cpcs 103-107 H19 imprinted maternally expressed transcript Homo sapiens 26-29 27062045-11 2016 In summary, melatonin antagonized premature senescence of CPCs via H19/miR-675/USP10 pathway, which provides new insights into pharmacological actions and potential applications of melatonin on the senescence of CPCs. Melatonin 12-21 H19 imprinted maternally expressed transcript Homo sapiens 67-70 27062045-11 2016 In summary, melatonin antagonized premature senescence of CPCs via H19/miR-675/USP10 pathway, which provides new insights into pharmacological actions and potential applications of melatonin on the senescence of CPCs. Melatonin 181-190 H19 imprinted maternally expressed transcript Homo sapiens 67-70 27349231-6 2016 In turn, trichostatin A, an HDAC inhibitor, significantly reduced CCCTC-binding factor (CTCF) occupancy in the imprinting control region upstream of the H19 gene locus and subsequently downregulated the expression of H19. trichostatin A 9-23 H19 imprinted maternally expressed transcript Homo sapiens 153-156 27349231-6 2016 In turn, trichostatin A, an HDAC inhibitor, significantly reduced CCCTC-binding factor (CTCF) occupancy in the imprinting control region upstream of the H19 gene locus and subsequently downregulated the expression of H19. trichostatin A 9-23 H19 imprinted maternally expressed transcript Homo sapiens 217-220 26729200-9 2016 CCAT2 rs6983267, H19 rs2839698, MALAT1 rs619586, and HOTAIR rs7958904 were associated with platinum-based chemotherapy response in dominant model ((P = 0.02, P = 0.04, P = 0.04, P = 0.01, respectively). Platinum 91-99 H19 imprinted maternally expressed transcript Homo sapiens 17-20 27346397-0 2016 [Mifepristone inhibites the migration of endometrial cancer cells through regulating H19 methylation]. Mifepristone 1-13 H19 imprinted maternally expressed transcript Homo sapiens 85-88 27346397-7 2016 In the Ishikawa cells, mifepristone suppressed the transcriptional level of H19 through enhancing its promoter methylation, which resulted in inhibited expressions of HMGA2 and vimentin and increased expression of E-cadherin in a time- and concentration-dependent manner. Mifepristone 23-35 H19 imprinted maternally expressed transcript Homo sapiens 76-79 27346397-8 2016 CONCLUSION: Mifepristone inhibits the migration of endometrial carcinoma cells partially through methylation-induced of transcriptional inhibition of H19, which results in the down-regulation of HMGA2 and vimentin and upregulation of E-cadherin. Mifepristone 12-24 H19 imprinted maternally expressed transcript Homo sapiens 150-153 27080438-0 2016 Prostacyclin-producing human mesenchymal cells target H19 lncRNA to augment endogenous progenitor function in hindlimb ischaemia. Epoprostenol 0-12 H19 imprinted maternally expressed transcript Homo sapiens 54-57 27193186-0 2016 The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer. Cisplatin 42-51 H19 imprinted maternally expressed transcript Homo sapiens 22-25 27193186-0 2016 The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer. Glutathione 77-88 H19 imprinted maternally expressed transcript Homo sapiens 22-25 27193186-4 2016 Here, we showed that expression of lin-RECK-3, H19, LUCAT1, LINC00961, and linc-CARS2-2 was enhanced in cisplatin-resistant A2780-DR cells, while transcriptome sequencing showed decreased Linc-TNFRSF19-1 and LINC00515 expression. Cisplatin 104-113 H19 imprinted maternally expressed transcript Homo sapiens 47-50 27193186-6 2016 H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Cisplatin 56-65 H19 imprinted maternally expressed transcript Homo sapiens 0-3 27193186-7 2016 Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Glutathione 140-151 H19 imprinted maternally expressed transcript Homo sapiens 188-191 27193186-8 2016 Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Hydrogen Peroxide 65-82 H19 imprinted maternally expressed transcript Homo sapiens 13-16 27193186-8 2016 Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. Glutathione 113-124 H19 imprinted maternally expressed transcript Homo sapiens 13-16 27193186-9 2016 Our results reveal a previously unknown link between H19 and glutathione metabolism in the regulation of cancer-drug resistance. Glutathione 61-72 H19 imprinted maternally expressed transcript Homo sapiens 53-56 26756094-5 2016 Plasma S-ASM activity correlated significantly with circulating markers of endothelial damage in the late-PE group (endoglin and sVCAM-1), with plasma cholesterol and total lipid levels. Cholesterol 151-162 H19 imprinted maternally expressed transcript Homo sapiens 9-12 27337854-4 2015 Overall uterotonic coverage was 82.5%: 85% of women who delivered at a facility received a uterotonic to prevent PPH; 76% of women reached at home at the time of birth by an ASM ingested misoprostol--a 44.3% coverage rate. Misoprostol 187-198 H19 imprinted maternally expressed transcript Homo sapiens 174-177 26171017-4 2015 Furthermore, MTT and Transwell assays revealed that overexpression of H19 in vitro promoted the proliferation and invasion of EC cell lines, whereas knockdown of H19 inhibited the proliferation and invasion of EC cell lines. monooxyethylene trimethylolpropane tristearate 13-16 H19 imprinted maternally expressed transcript Homo sapiens 70-73 26386650-3 2015 Regulation of imprinting of H19 and IGF2 was determined by the DNA methylation status at three CpG sites within the H19 imprinting control region 1 (ICR1) using bisulphite pyrosequencing. hydrogen sulfite 161-171 H19 imprinted maternally expressed transcript Homo sapiens 28-31 26386650-3 2015 Regulation of imprinting of H19 and IGF2 was determined by the DNA methylation status at three CpG sites within the H19 imprinting control region 1 (ICR1) using bisulphite pyrosequencing. hydrogen sulfite 161-171 H19 imprinted maternally expressed transcript Homo sapiens 116-119 25707431-0 2015 5-Azacytidine inhibits human rhabdomyosarcoma cell growth by downregulating insulin-like growth factor 2 expression and reactivating the H19 gene product miR-675, which negatively affects insulin-like growth factors and insulin signaling. Azacitidine 0-13 H19 imprinted maternally expressed transcript Homo sapiens 137-140 25846769-0 2015 H19 lncRNA mediates 17beta-estradiol-induced cell proliferation in MCF-7 breast cancer cells. 17beta 20-26 H19 imprinted maternally expressed transcript Homo sapiens 0-3 25846769-0 2015 H19 lncRNA mediates 17beta-estradiol-induced cell proliferation in MCF-7 breast cancer cells. Estradiol 27-36 H19 imprinted maternally expressed transcript Homo sapiens 0-3 25846769-5 2015 17beta-estradiol produced a dose- and time-dependent induction of H19 expression in MCF-7 cells, which was mediated via ERalpha as evident by the blockade of this 17beta-estradiol effect with ICI 182780, a specific ER antagonist and knockdown of ERalpha using specific RNAi. Estradiol 0-16 H19 imprinted maternally expressed transcript Homo sapiens 66-69 25846769-5 2015 17beta-estradiol produced a dose- and time-dependent induction of H19 expression in MCF-7 cells, which was mediated via ERalpha as evident by the blockade of this 17beta-estradiol effect with ICI 182780, a specific ER antagonist and knockdown of ERalpha using specific RNAi. Estradiol 163-179 H19 imprinted maternally expressed transcript Homo sapiens 66-69 25707431-5 2015 We observed that AzaC-mediated demethylation of the DMR at the IGF2-H19 locus resulted in downregulation of IGF2 and an increase in the expression of H19. Azacitidine 17-21 H19 imprinted maternally expressed transcript Homo sapiens 68-71 25707431-5 2015 We observed that AzaC-mediated demethylation of the DMR at the IGF2-H19 locus resulted in downregulation of IGF2 and an increase in the expression of H19. Azacitidine 17-21 H19 imprinted maternally expressed transcript Homo sapiens 150-153 26091021-5 2015 Using specific techniques to map 5mC and 5hmC at DMRs controlling the expression of CDKN1C and the imprinted gene IGF2, we show that 5mC enrichment at KvDMR and DMR0, and 5hmC enrichment within the H19 gene body, associate positively with birth weight. 5-Methylcytidine 5'-monophosphate 133-136 H19 imprinted maternally expressed transcript Homo sapiens 198-201 25855965-1 2015 We previously reported that IL-2 deprivation induced acid sphingomyelinase-mediated (ASM-mediated) ceramide elevation and apoptosis in an NK/T lymphoma cell line KHYG-1. Ceramides 99-107 H19 imprinted maternally expressed transcript Homo sapiens 85-88 25855965-5 2015 However, IL-2 deprivation induced ceramide elevation via ASM in lysosomes and activated lysosomal cathepsin B (CTSB) but not cathepsin D. Ceramides 34-42 H19 imprinted maternally expressed transcript Homo sapiens 57-60 25855965-7 2015 Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome. Ceramides 14-22 H19 imprinted maternally expressed transcript Homo sapiens 58-61 25855965-7 2015 Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome. Desipramine 73-84 H19 imprinted maternally expressed transcript Homo sapiens 58-61 25855965-10 2015 These findings suggest that lysosomal ceramide produced by ASM mediates XIAP degradation by activation of cytosolic CTSB and caspase-dependent apoptosis. Ceramides 38-46 H19 imprinted maternally expressed transcript Homo sapiens 59-62 25855965-11 2015 The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells. Ceramides 8-16 H19 imprinted maternally expressed transcript Homo sapiens 4-7 25855965-11 2015 The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells. Ceramides 59-67 H19 imprinted maternally expressed transcript Homo sapiens 4-7 24299031-0 2014 A novel de novo point mutation of the OCT-binding site in the IGF2/H19-imprinting control region in a Beckwith-Wiedemann syndrome patient. maxacalcitol 38-41 H19 imprinted maternally expressed transcript Homo sapiens 67-70 25487127-1 2014 Gold-silver core-shell nanoparticles stabilized with a common sweetener, aspartame (AuNP@Ag@Asm), combine the antimicrobial properties of silver with the photoinduced plasmon-mediated photothermal effects of gold. Aspartame 73-82 H19 imprinted maternally expressed transcript Homo sapiens 92-95 25487127-1 2014 Gold-silver core-shell nanoparticles stabilized with a common sweetener, aspartame (AuNP@Ag@Asm), combine the antimicrobial properties of silver with the photoinduced plasmon-mediated photothermal effects of gold. aunp 84-88 H19 imprinted maternally expressed transcript Homo sapiens 92-95 25487127-1 2014 Gold-silver core-shell nanoparticles stabilized with a common sweetener, aspartame (AuNP@Ag@Asm), combine the antimicrobial properties of silver with the photoinduced plasmon-mediated photothermal effects of gold. Silver 5-11 H19 imprinted maternally expressed transcript Homo sapiens 92-95 25293351-0 2014 Dietary supplementation with polyunsaturated fatty acid during pregnancy modulates DNA methylation at IGF2/H19 imprinted genes and growth of infants. Fatty Acids, Unsaturated 29-55 H19 imprinted maternally expressed transcript Homo sapiens 107-110 25293351-7 2014 In addition, at H19 DMR, methylation levels were significantly lower in the DHA group than the control group in infants of normal weight mothers (P = 0.01). Docosahexaenoic Acids 76-79 H19 imprinted maternally expressed transcript Homo sapiens 16-19 24471656-5 2014 In enzymatically dissociated human ASM cells loaded with the Ca(2+) indicator, fura-2, AA (1-10 muM) triggered [Ca(2+)]i oscillations that were inhibited by removal of extracellular Ca(2+). Fura-2 79-85 H19 imprinted maternally expressed transcript Homo sapiens 35-38 24972507-0 2014 The impact of first trimester phthalate and phenol exposure on IGF2/H19 genomic imprinting and birth outcomes. phthalic acid 30-39 H19 imprinted maternally expressed transcript Homo sapiens 68-71 24972507-0 2014 The impact of first trimester phthalate and phenol exposure on IGF2/H19 genomic imprinting and birth outcomes. Phenol 44-50 H19 imprinted maternally expressed transcript Homo sapiens 68-71 24972507-12 2014 However increased deviation of allele-specific expression of H19 was associated with Sigmadi(2-ethylhexyl) phthalate metabolites and high molecular weight phthalates. sigmadi(2-ethylhexyl) phthalate 85-116 H19 imprinted maternally expressed transcript Homo sapiens 61-64 24253175-7 2014 Striking responses were seen to vadimezan with an IC50 of 90 and 150 mug/ml for ASM and ISO-HAS cells, respectively. vadimezan 32-41 H19 imprinted maternally expressed transcript Homo sapiens 80-83 24685695-5 2014 Silencing H19 expression sensitized leukemic cells to undergo imatinib-induced apoptosis and inhibited Bcr-Abl-induced tumor growth. Imatinib Mesylate 62-70 H19 imprinted maternally expressed transcript Homo sapiens 10-13 24671855-10 2014 MTT and colony formation assays confirmed that H19 expression affects GC cell proliferation in vitro. monooxyethylene trimethylolpropane tristearate 0-3 H19 imprinted maternally expressed transcript Homo sapiens 47-50 23943562-0 2014 H19 DMR methylation correlates to the progression of esophageal squamous cell carcinoma through IGF2 imprinting pathway. aspartylmethionylarginine 4-7 H19 imprinted maternally expressed transcript Homo sapiens 0-3 23943562-5 2014 Methylation status of H19 DMR in informative samples was analyzed by bisulfite sequencing PCR. hydrogen sulfite 69-78 H19 imprinted maternally expressed transcript Homo sapiens 22-25 24253175-8 2014 Selumetinib inhibited ASM with an IC50 of 1,750 ng/ml, but was not effective in ISO-HAS. AZD 6244 0-11 H19 imprinted maternally expressed transcript Homo sapiens 22-25 24253175-9 2014 Everolimus reduced both ASM and ISO-HAS viable cell counts by 20 % (p < 0.001). Everolimus 0-10 H19 imprinted maternally expressed transcript Homo sapiens 24-27 24253175-10 2014 Minimal responses were observed to bevacizumab and axitinib in assays with ASM and ISO-HAS cells. Axitinib 51-59 H19 imprinted maternally expressed transcript Homo sapiens 75-78 24761865-0 2014 Aflatoxin B1 promotes cell growth and invasion in hepatocellular carcinoma HepG2 cells through H19 and E2F1. Aflatoxin B1 0-12 H19 imprinted maternally expressed transcript Homo sapiens 95-98 24188929-3 2014 However, little is known about their toxic or beneficial effects on human health, especially in the respiratory system, where its smooth muscle (ASM) regulates the airway contractility by different mediators, such as acetylcholine (ACh) and nitric oxide (NO). Nitric Oxide 241-253 H19 imprinted maternally expressed transcript Homo sapiens 145-148 24188929-3 2014 However, little is known about their toxic or beneficial effects on human health, especially in the respiratory system, where its smooth muscle (ASM) regulates the airway contractility by different mediators, such as acetylcholine (ACh) and nitric oxide (NO). Acetylcholine 217-230 H19 imprinted maternally expressed transcript Homo sapiens 145-148 24188929-3 2014 However, little is known about their toxic or beneficial effects on human health, especially in the respiratory system, where its smooth muscle (ASM) regulates the airway contractility by different mediators, such as acetylcholine (ACh) and nitric oxide (NO). Acetylcholine 232-235 H19 imprinted maternally expressed transcript Homo sapiens 145-148 24761865-6 2014 In addition, AFB1 induced the expression of E2F1 and its knock-down could down-regulate H19 expression and suppress cell growth and invasion in hepatocellular carcinoma HepG2 cells. Aflatoxin B1 13-17 H19 imprinted maternally expressed transcript Homo sapiens 88-91 24761865-8 2014 In summary, our results suggested that aflatoxin B1 could promote cell growth and invasion in hepatocellular carcinoma HepG2 cells through actions on H19 and E2F1. Aflatoxin B1 39-51 H19 imprinted maternally expressed transcript Homo sapiens 150-153 25660404-8 2014 Stimulation of basophils with anti-IgE increased CD203c expression and histamine release, which was inhibited by ASM-024 (10(-5) to 10(-)(3) M, p < 0.05). Histamine 71-80 H19 imprinted maternally expressed transcript Homo sapiens 113-116 25049758-8 2013 In the case of the imprinting genes H19 and NNAT, except PEG1, the SCNT blastocysts both with and without TSA treatment showed higher levels than those of the in vivo blastocysts. trichostatin A 106-109 H19 imprinted maternally expressed transcript Homo sapiens 36-39 24044616-0 2013 Comment on "Modeling nitrous oxide production during biological nitrogen removal via nitrification and denitrification: extensions to the general asm models". Nitrous Oxide 21-34 H19 imprinted maternally expressed transcript Homo sapiens 146-149 24044616-0 2013 Comment on "Modeling nitrous oxide production during biological nitrogen removal via nitrification and denitrification: extensions to the general asm models". Nitrogen 64-72 H19 imprinted maternally expressed transcript Homo sapiens 146-149 24044636-0 2013 Reply to comment on "Modeling nitrous oxide production during biological nitrogen removal via nitrification and denitrification: extensions to the general asm models". Nitrous Oxide 30-43 H19 imprinted maternally expressed transcript Homo sapiens 155-158 24044636-0 2013 Reply to comment on "Modeling nitrous oxide production during biological nitrogen removal via nitrification and denitrification: extensions to the general asm models". Nitrogen 73-81 H19 imprinted maternally expressed transcript Homo sapiens 155-158 22542538-11 2012 RESULTS: Propofol was present in ASM caveolar fractions in substantial concentrations. Propofol 9-17 H19 imprinted maternally expressed transcript Homo sapiens 33-36 23585276-4 2013 In this study, we set out to determine whether 5-AzaCdR treatment can reprogram the epigenomic organization of the IGF2-H19 locus in a choriocarcinoma cancer cell line (JEG3). 5-azacdr 47-55 H19 imprinted maternally expressed transcript Homo sapiens 120-123 23585276-5 2013 We found that localized DNA demethylation at the H19 imprinting control region (ICR) induced by 5-AzaCdR, reduced IGF2, increased H19 expression, increased CTCF and cohesin recruitment and changed histone modifications. 5-azacdr 96-104 H19 imprinted maternally expressed transcript Homo sapiens 49-52 22542538-18 2012 Due to its lipid nature, propofol may transiently disrupt caveolar regulation, thus altering ASM [Ca(2+)](i). Propofol 25-33 H19 imprinted maternally expressed transcript Homo sapiens 93-96 23927428-3 2013 To develop a new control strategy, the potential for 1,2,3-benzothiadiazole-7-thiocarboxylic acid-S-methyl-ester (ASM) to suppress CCYV infection was evaluated. 1,2,3-benzothiadiazole-7-thiocarboxylic acid-s-methyl-ester 53-112 H19 imprinted maternally expressed transcript Homo sapiens 114-117 23805108-10 2013 RESULTS: There were significant differences in the change of %5-mC pre- to post-deployment between cases and controls for H19 (cases: +0.57%, controls: -1.97%; p = 0.04) and IL18 (cases: +1.39%, controls: -3.83%; p = 0.01). 5-mc 62-66 H19 imprinted maternally expressed transcript Homo sapiens 122-125 23805108-13 2013 CONCLUSION: In the study of deployed personnel, those who did not develop PTSD had reduced %5-mC levels of H19 and IL18 after deployment, while those who did develop PTSD had increased levels of IL18. 5-mc 92-96 H19 imprinted maternally expressed transcript Homo sapiens 107-110 23660367-7 2013 As a potential mechanism underlying this disrupted expression, the methylation of Igf2/H19 DMR3 was detected using bisulfite sequencing PCR analysis, which revealed the significant hypomethylation of DMR3 in parthenogenetic fetuses and placentas. hydrogen sulfite 115-124 H19 imprinted maternally expressed transcript Homo sapiens 87-90 22016308-9 2012 Co-incubation of rings with radicicol and estradiol produced an ER-dependent increase in the relaxation response to SNP of both normal and asthmatic ASM. monorden 28-37 H19 imprinted maternally expressed transcript Homo sapiens 149-152 22016308-9 2012 Co-incubation of rings with radicicol and estradiol produced an ER-dependent increase in the relaxation response to SNP of both normal and asthmatic ASM. Estradiol 42-51 H19 imprinted maternally expressed transcript Homo sapiens 149-152 22016308-10 2012 Estrogen-induced relaxation of ASM was abolished by overnight incubation with radicicol and this was associated with reduced expression of ERbeta. monorden 78-87 H19 imprinted maternally expressed transcript Homo sapiens 31-34 22993648-2 2012 Single promoter vectors expressing diphtheria toxin A-fragment (DTA) under the control regulation of IGF2-P4 or H19 regulatory sequences (IGF2-P4-DTA and H19-DTA) were previously successfully used in cell lines, animal models and recently in human patients with superficial cell carcinoma of the bladder, pancreatic cancer and ovarian cancer (treated with H19-DTA). diphtheria toxin fragment A 64-67 H19 imprinted maternally expressed transcript Homo sapiens 112-115 22427002-7 2012 Hypomethylation of the sixth CTCF-binding site in the DMR of IGF2/H19 is linked to LOI and the common IGF2-H19 enhancer competition model for IGF2 imprinting does not apply to human CRC. ctcf 29-33 H19 imprinted maternally expressed transcript Homo sapiens 66-69 22427002-7 2012 Hypomethylation of the sixth CTCF-binding site in the DMR of IGF2/H19 is linked to LOI and the common IGF2-H19 enhancer competition model for IGF2 imprinting does not apply to human CRC. ctcf 29-33 H19 imprinted maternally expressed transcript Homo sapiens 107-110 21768203-8 2012 Whereas 5-azacytidine significantly increased the mRNA expression of the epigenetically regulated gene H19, TLR2 expression was not affected. Azacitidine 8-21 H19 imprinted maternally expressed transcript Homo sapiens 103-106 22567173-3 2012 Recently we reported that a single construct that expresses DTA under the control of both H19 and IGF2 P4 promoters showed superior efficacy in vitro as well as in vivo, in comparison to a single promoter construct in bladder carcinoma. diphtheria toxin fragment A 60-63 H19 imprinted maternally expressed transcript Homo sapiens 90-93 22567173-4 2012 Here we extended this approach to glioblastoma and tested the antitumor efficacy of the double promoter DTA-expressing vector (H19-DTA-P4-DTA) in vitro as well as in heterotopic animal model. diphtheria toxin fragment A 104-107 H19 imprinted maternally expressed transcript Homo sapiens 127-130 22567173-4 2012 Here we extended this approach to glioblastoma and tested the antitumor efficacy of the double promoter DTA-expressing vector (H19-DTA-P4-DTA) in vitro as well as in heterotopic animal model. dta-p4-dta 131-141 H19 imprinted maternally expressed transcript Homo sapiens 127-130 22993648-7 2012 RESULTS: The double promoter vector exhibited superior inhibition activity compared to the single promoter expression vectors, in the different cancer cell lines furthermore, the double promoter vector H19-DTA-P4-DTA exhibited augmented-than-additive anti-cancer activity relative to single promoter expression vectors carrying either DTA sequence alone, when tested in a broad spectrum of tumor cells. dta-p4-dta 206-216 H19 imprinted maternally expressed transcript Homo sapiens 202-205 22993648-7 2012 RESULTS: The double promoter vector exhibited superior inhibition activity compared to the single promoter expression vectors, in the different cancer cell lines furthermore, the double promoter vector H19-DTA-P4-DTA exhibited augmented-than-additive anti-cancer activity relative to single promoter expression vectors carrying either DTA sequence alone, when tested in a broad spectrum of tumor cells. diphtheria toxin fragment A 206-209 H19 imprinted maternally expressed transcript Homo sapiens 202-205 21573965-1 2011 This study was designed to test the hypothesis that polymorphic variation in maternally transmitted foetal H19 alleles is associated with offspring size at birth and alterations in maternal glucose concentrations in pregnancy. Glucose 190-197 H19 imprinted maternally expressed transcript Homo sapiens 107-110 21908411-11 2011 CONCLUSIONS: Lower vitamin D levels in children with STRA were associated with increased ASM mass and worse asthma control and lung function. Vitamin D 19-28 H19 imprinted maternally expressed transcript Homo sapiens 89-92 21874233-6 2011 All of the tumors treated with the control vector increased in size, whereas 35.7% of the tumors in the groups treated with a total amount of 2.5 mg DTA-H19 plasmid shrank in size. deoxythymidylyl-3'-5'-deoxyadenylate 149-152 H19 imprinted maternally expressed transcript Homo sapiens 153-156 21340676-4 2011 In this study, a slightly modified ASM1 model was implemented in the GPS-X software to simulate the concentration of such intermediate products (NO2-, NO and N2O) and to estimate the amounts of gaseous N2O emitted by the denitrification stage (12 biofilters) of the Seine-Centre WWTP (SIAAP, Paris). Nitrogen Dioxide 145-148 H19 imprinted maternally expressed transcript Homo sapiens 35-39 21340676-4 2011 In this study, a slightly modified ASM1 model was implemented in the GPS-X software to simulate the concentration of such intermediate products (NO2-, NO and N2O) and to estimate the amounts of gaseous N2O emitted by the denitrification stage (12 biofilters) of the Seine-Centre WWTP (SIAAP, Paris). Nitrous Oxide 158-161 H19 imprinted maternally expressed transcript Homo sapiens 35-39 21340676-4 2011 In this study, a slightly modified ASM1 model was implemented in the GPS-X software to simulate the concentration of such intermediate products (NO2-, NO and N2O) and to estimate the amounts of gaseous N2O emitted by the denitrification stage (12 biofilters) of the Seine-Centre WWTP (SIAAP, Paris). Nitrous Oxide 202-205 H19 imprinted maternally expressed transcript Homo sapiens 35-39 21515660-8 2011 Overnight (24 h) exposure of ASM cells to 50% oxygen increased BDNF and TrkB expression and potentiated both SP- and BDNF-induced enhancement of [Ca(2+)](i) (P < 0.05). Oxygen 46-52 H19 imprinted maternally expressed transcript Homo sapiens 29-32 19338988-11 2010 CONCLUSION(S): Testicular spermatozoa from men with abnormal spermatogenesis carry methylation defects in the H19 imprinted gene which also affect the CTCF-binding site, further supporting an association between the occurrence of imprinting errors and disruptive spermatogenesis. ctcf 151-155 H19 imprinted maternally expressed transcript Homo sapiens 110-113 21991322-6 2011 Specifically, for the first time we showed that the rs10732516 [A] polymorphism, located in a critical CTCF binding site in the H19 ICR locus, is strongly associated with increased hypermethylation of specific CpG sites in the maternal H19 allele. ctcf 103-107 H19 imprinted maternally expressed transcript Homo sapiens 128-131 21991322-6 2011 Specifically, for the first time we showed that the rs10732516 [A] polymorphism, located in a critical CTCF binding site in the H19 ICR locus, is strongly associated with increased hypermethylation of specific CpG sites in the maternal H19 allele. ctcf 103-107 H19 imprinted maternally expressed transcript Homo sapiens 236-239 19496980-2 2010 We report a case of BWS in a girl with unresectable hepatoblastoma, who received a planned LVDT following neo-adjuvant chemotherapy. lvdt 91-95 H19 imprinted maternally expressed transcript Homo sapiens 20-23 21726155-1 2011 A simple and accurate method for the analysis of acibenzolar-S-methyl (benzo[1,2,3]thiadiazole-7-carbothioic acid-S-methyl ester; CGA 245 704; ASM) and its major conversion product, benzo[1,2,3]thiadiazole-7-carboxylic acid (CGA 210 007; BTC), in soils is presented. S-methyl benzo(1,2,3)thiadiazole-7-carbothioate 71-128 H19 imprinted maternally expressed transcript Homo sapiens 143-146 21726155-2 2011 ASM extraction from soil samples was performed using acetonitrile and BTC was extracted with a mixture of potassium phosphate buffer (0.5 M, pH 3) and acetonitrile (70:30 %, v/v). acetonitrile 53-65 H19 imprinted maternally expressed transcript Homo sapiens 0-3 21726155-2 2011 ASM extraction from soil samples was performed using acetonitrile and BTC was extracted with a mixture of potassium phosphate buffer (0.5 M, pH 3) and acetonitrile (70:30 %, v/v). btc 70-73 H19 imprinted maternally expressed transcript Homo sapiens 0-3 21726155-2 2011 ASM extraction from soil samples was performed using acetonitrile and BTC was extracted with a mixture of potassium phosphate buffer (0.5 M, pH 3) and acetonitrile (70:30 %, v/v). potassium phosphate 106-125 H19 imprinted maternally expressed transcript Homo sapiens 0-3 21726155-2 2011 ASM extraction from soil samples was performed using acetonitrile and BTC was extracted with a mixture of potassium phosphate buffer (0.5 M, pH 3) and acetonitrile (70:30 %, v/v). acetonitrile 151-163 H19 imprinted maternally expressed transcript Homo sapiens 0-3 21858195-8 2011 In fura-2 loaded human ASM cells, NCX-mediated inward Ca(2+) exchange as well as outward exchange (measured as rates of change in [Ca(2+)](i)) was elicited by altering extracellular Na(+) and Ca(2+) levels. Fura-2 3-9 H19 imprinted maternally expressed transcript Homo sapiens 23-26 19933149-4 2009 Moreover, CTCF-binding sites within the H19 imprinting control region (ICR) not only determine the physical proximity among imprinted domains, but also transvect allele-specific epigenetic states, identified by replication timing patterns, to interacting, nonallelic imprinted regions during germline development. ctcf 10-14 H19 imprinted maternally expressed transcript Homo sapiens 40-43 20418490-6 2010 Furthermore, we found that a significant fraction (38%-88%) of ASM regions is dependent on the presence of heterozygous SNPs in CpG dinucleotides that disrupt their methylation potential. cytidylyl-3'-5'-guanosine 128-145 H19 imprinted maternally expressed transcript Homo sapiens 63-66 19362547-10 2009 Betaine, another methyl group donor, prevented only H19 and AIR up regulation induced by DDC, on microarrays. Betaine 0-7 H19 imprinted maternally expressed transcript Homo sapiens 52-55 19814617-5 2009 In the present study, we investigated a possible method of quantitatively determining H19 hypomethylation in RSS patients using a combined bisulfite restriction analysis (COBRA)-denaturing high-performance liquid chromatography (DHPLC) assay; in this combined assay, polymerase chain reaction products amplified from the H19 differentially methylated region of bisulfite-treated genomic DNA were analyzed using a COBRA assay, which detects methylation-dependent sequence differences in the bisulfite-treated genomic DNA using a restriction enzyme analysis. hydrogen sulfite 139-148 H19 imprinted maternally expressed transcript Homo sapiens 86-89 19814617-5 2009 In the present study, we investigated a possible method of quantitatively determining H19 hypomethylation in RSS patients using a combined bisulfite restriction analysis (COBRA)-denaturing high-performance liquid chromatography (DHPLC) assay; in this combined assay, polymerase chain reaction products amplified from the H19 differentially methylated region of bisulfite-treated genomic DNA were analyzed using a COBRA assay, which detects methylation-dependent sequence differences in the bisulfite-treated genomic DNA using a restriction enzyme analysis. hydrogen sulfite 361-370 H19 imprinted maternally expressed transcript Homo sapiens 86-89 19814617-5 2009 In the present study, we investigated a possible method of quantitatively determining H19 hypomethylation in RSS patients using a combined bisulfite restriction analysis (COBRA)-denaturing high-performance liquid chromatography (DHPLC) assay; in this combined assay, polymerase chain reaction products amplified from the H19 differentially methylated region of bisulfite-treated genomic DNA were analyzed using a COBRA assay, which detects methylation-dependent sequence differences in the bisulfite-treated genomic DNA using a restriction enzyme analysis. hydrogen sulfite 361-370 H19 imprinted maternally expressed transcript Homo sapiens 86-89 19834551-5 2009 Ceramides induced by MV, but also bacterial sphingomyelinase, efficiently interfered with formation of membrane protrusions and T cell spreading and front/rear polarisation in response to beta1 integrin ligation or alphaCD3/CD28 activation, and this was rescued upon pharmacological or genetic ablation of ASM/NSM activity. Ceramides 0-9 H19 imprinted maternally expressed transcript Homo sapiens 306-309 19519716-0 2009 Effect of alcohol consumption on CpG methylation in the differentially methylated regions of H19 and IG-DMR in male gametes: implications for fetal alcohol spectrum disorders. Alcohols 10-17 H19 imprinted maternally expressed transcript Homo sapiens 93-96 19519716-9 2009 CpG site #4 in the IG-DMR was preferentially demethylated among all individuals and along with the H19 DMR CpG site #7 located within the CTCF binding site 6 showed significant demethylation in the alcohol consuming groups compared with the control group. aspartylmethionylarginine 22-25 H19 imprinted maternally expressed transcript Homo sapiens 99-102 19519716-9 2009 CpG site #4 in the IG-DMR was preferentially demethylated among all individuals and along with the H19 DMR CpG site #7 located within the CTCF binding site 6 showed significant demethylation in the alcohol consuming groups compared with the control group. Alcohols 198-205 H19 imprinted maternally expressed transcript Homo sapiens 99-102 19656414-7 2009 Intratumoral injection of DTA-H19 into ectopically developed tumors caused 40% inhibition of tumor growth. deoxythymidylyl-3'-5'-deoxyadenylate 26-29 H19 imprinted maternally expressed transcript Homo sapiens 30-33 19499149-4 2009 This study aims to investigate the potential impact of Hcy on gene imprinting of IGF2 and H19. Homocysteine 55-58 H19 imprinted maternally expressed transcript Homo sapiens 90-93 19513555-0 2009 Aberrant epigenetic modifications in the CTCF binding domain of the IGF2/H19 gene in prostate cancer compared with benign prostate hyperplasia. ctcf 41-45 H19 imprinted maternally expressed transcript Homo sapiens 73-76 19513555-10 2009 We observed statistically significant differences in the methylation state between PCa and BPH groups, especially in the DMR of H19 (p<0.0001) and in the ICR (p=0.0034), which corresponds to CTCF binding domain. aspartylmethionylarginine 121-124 H19 imprinted maternally expressed transcript Homo sapiens 128-131 19513555-10 2009 We observed statistically significant differences in the methylation state between PCa and BPH groups, especially in the DMR of H19 (p<0.0001) and in the ICR (p=0.0034), which corresponds to CTCF binding domain. ctcf 194-198 H19 imprinted maternally expressed transcript Homo sapiens 128-131 19499149-8 2009 The results showed that the Hcy treatment resulted in hypomethylation of the sixth CTCF-binding site upstream of H19 of VSMCs. Homocysteine 28-31 H19 imprinted maternally expressed transcript Homo sapiens 113-116 19499149-9 2009 The expression of H19 was increased, whereas the IGF2 mRNA and protein were decreased, the CTCF expression increased with the increase in Hcy concentration. Homocysteine 138-141 H19 imprinted maternally expressed transcript Homo sapiens 18-21 19499149-10 2009 These data indicated that Hcy could induce hypomethylation of the sixth CTCF-binding sites upstream of H19, which is an important regulating area for the imprinting expression of IGF2 and H19. Homocysteine 26-29 H19 imprinted maternally expressed transcript Homo sapiens 103-106 19499149-10 2009 These data indicated that Hcy could induce hypomethylation of the sixth CTCF-binding sites upstream of H19, which is an important regulating area for the imprinting expression of IGF2 and H19. Homocysteine 26-29 H19 imprinted maternally expressed transcript Homo sapiens 188-191 18348204-8 2008 Monoallelic IGF2 expression was maintained in curcumin-treated cancer cells, indicating the involvement of mechanism/s other than disturbance of CTCF insulator function at the IGF2/H19 locus. Curcumin 46-54 H19 imprinted maternally expressed transcript Homo sapiens 181-184 18348204-0 2008 Curcumin downregulates H19 gene transcription in tumor cells. Curcumin 0-8 H19 imprinted maternally expressed transcript Homo sapiens 23-26 18159214-2 2008 In 30% of patients, the differentially methylated IGF2/H19 imprinting center region (ICR1) on chromosome 11p15 was found to be hypomethylated, as determined by Southern blot analysis of an HpaII restriction site close to the third CTCF-binding site (CTS3) within ICR1. ctcf 231-235 H19 imprinted maternally expressed transcript Homo sapiens 55-58 18348204-6 2008 As expression of imprinted genes is often altered in tumors, we investigated the potential effect of curcumin treatment on transcription of the imprinted H19 gene, located distally from the CTCF binding site, in human tumor cell lines HCT 116, SW 620, HeLa, Cal 27, Hep-2 and Detroit 562. Curcumin 101-109 H19 imprinted maternally expressed transcript Homo sapiens 154-157 18501891-7 2008 Moreover, we analyzed the methylation state of the promoter regions of H19, PHLDA2, and SLC22A18 genes by bisulfite sequencing array and observed a correlation between upregulated expression of H19 and PHLDA2 genes and hypomethylation of their promoter regions, although this was not observed for SLC22A18. hydrogen sulfite 106-115 H19 imprinted maternally expressed transcript Homo sapiens 71-74 18501891-7 2008 Moreover, we analyzed the methylation state of the promoter regions of H19, PHLDA2, and SLC22A18 genes by bisulfite sequencing array and observed a correlation between upregulated expression of H19 and PHLDA2 genes and hypomethylation of their promoter regions, although this was not observed for SLC22A18. hydrogen sulfite 106-115 H19 imprinted maternally expressed transcript Homo sapiens 194-197 18556436-10 2008 We conclude that the normal bronchodilatory response to DI occurs as a result of the direct mechanical effects of DI on activated ASM in the airway wall. di 56-58 H19 imprinted maternally expressed transcript Homo sapiens 130-133 18556436-10 2008 We conclude that the normal bronchodilatory response to DI occurs as a result of the direct mechanical effects of DI on activated ASM in the airway wall. di 114-116 H19 imprinted maternally expressed transcript Homo sapiens 130-133 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 136-147 H19 imprinted maternally expressed transcript Homo sapiens 0-3 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 136-147 H19 imprinted maternally expressed transcript Homo sapiens 45-48 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 182-193 H19 imprinted maternally expressed transcript Homo sapiens 0-3 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 182-193 H19 imprinted maternally expressed transcript Homo sapiens 45-48 17237358-2 2007 Here, we identify a 23-nucleotide microRNA derived from H19 that is endogenously expressed in human keratinocytes and neonatal mice and overexpressed in cells transfected with human or mouse H19 expression plasmids. 23-nucleotide 20-33 H19 imprinted maternally expressed transcript Homo sapiens 56-59 16532746-7 2006 The oxygen/nitrate return sludge model block predicts a 10% improvement of N removal performance under dynamic conditions, and might be the better modelling option for ASM1 plants: it is computationally more efficient and it will not overrate the importance of decay processes in the settler. Oxygen 4-10 H19 imprinted maternally expressed transcript Homo sapiens 168-172 17564365-6 2007 In order to model the nitrite accumulation observed, the ASM1 model was extended with a two-step nitrification and denitrification including nitrite as intermediate. Nitrites 22-29 H19 imprinted maternally expressed transcript Homo sapiens 57-61 17564365-6 2007 In order to model the nitrite accumulation observed, the ASM1 model was extended with a two-step nitrification and denitrification including nitrite as intermediate. Nitrites 141-148 H19 imprinted maternally expressed transcript Homo sapiens 57-61 16428269-5 2006 The Cl(-) channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10(-4) M), previously shown to inhibit SR Cl(-) channels, significantly reduced the magnitude of successive acetylcholine-induced contractions of airway smooth muscle (ASM), suggesting a "run down" of sequestered Ca(2+) within the SR. Niflumic acid (10(-4) M), a structurally different Cl(-) channel blocker, had no such effect. 5-nitro-2-(3-phenylpropylamino)benzoic acid 26-69 H19 imprinted maternally expressed transcript Homo sapiens 245-248 16428269-7 2006 Depletion of Cl(i)(-), accomplished by bathing ASM strips in Cl(-)-free buffer, significantly reduced the magnitude of successive acetylcholine-induced contractions. Acetylcholine 130-143 H19 imprinted maternally expressed transcript Homo sapiens 47-50 16707479-7 2006 The imprinted gene H19 showed little change in methylation after decitabine. Decitabine 65-75 H19 imprinted maternally expressed transcript Homo sapiens 19-22 16532746-7 2006 The oxygen/nitrate return sludge model block predicts a 10% improvement of N removal performance under dynamic conditions, and might be the better modelling option for ASM1 plants: it is computationally more efficient and it will not overrate the importance of decay processes in the settler. Nitrates 11-18 H19 imprinted maternally expressed transcript Homo sapiens 168-172 16532746-7 2006 The oxygen/nitrate return sludge model block predicts a 10% improvement of N removal performance under dynamic conditions, and might be the better modelling option for ASM1 plants: it is computationally more efficient and it will not overrate the importance of decay processes in the settler. Nitrogen 75-76 H19 imprinted maternally expressed transcript Homo sapiens 168-172 15013932-1 2004 Pimecrolimus (SDZ ASM 981, Elidel ) is an ascomycin macrolactam derivative and a cell-selective inhibitor of inflammatory cytokines specifically developed to treat inflammatory skin diseases. pimecrolimus 0-12 H19 imprinted maternally expressed transcript Homo sapiens 18-21 15885138-7 2005 Study of the independent Cambridge birth cohort with available DNA in mothers (N = 646) provided additional support for mother"s H19 2992 genotype associations with birthweight (P = 0.04) and with mother"s glucose levels (P = 0.01) in first pregnancies. Glucose 206-213 H19 imprinted maternally expressed transcript Homo sapiens 129-132 16331412-2 2005 Imprinting of a structurally homologous region IGF2/H19 on 11p15 is mediated through cytosine methylation-controlled binding of the protein CTCF to target sites upstream of H19. Cytosine 85-93 H19 imprinted maternally expressed transcript Homo sapiens 52-55 16331412-2 2005 Imprinting of a structurally homologous region IGF2/H19 on 11p15 is mediated through cytosine methylation-controlled binding of the protein CTCF to target sites upstream of H19. Cytosine 85-93 H19 imprinted maternally expressed transcript Homo sapiens 173-176 16206856-11 2005 Therefore, it is concluded that the ASM1 based sewer model properly describes the changes in dissolved oxygen level in an aerobic sewer reach. Oxygen 103-109 H19 imprinted maternally expressed transcript Homo sapiens 36-40 15351705-6 2004 We also found that 5-AzaC demethylated the promoter region of H19 gene, a typical methylated gene during embryonic differentiation. Azacitidine 19-25 H19 imprinted maternally expressed transcript Homo sapiens 62-65 15240554-5 2004 Following culture in Whitten"s medium, the normally silent paternal H19 allele was aberrantly expressed and undermethylated. whitten"s medium 21-37 H19 imprinted maternally expressed transcript Homo sapiens 68-71 16189152-2 2005 METHODS: Non-radioactive in situ hybridisation for H19 RNA was performed on paraffin wax embedded sections of liver biopsies or partial hepatectomy specimens, taken from 80 patients with hepatic metastases derived from carcinomas from several medical centres in Israel. Paraffin 76-88 H19 imprinted maternally expressed transcript Homo sapiens 51-54 15525575-5 2004 PRL and DHT appeared to be opposite mediators in the H19 RNA synthesis. Dihydrotestosterone 8-11 H19 imprinted maternally expressed transcript Homo sapiens 53-56 15525575-11 2004 We conclude that H19 expression is regulated by both a peptidic and a male steroid hormone. Steroids 75-82 H19 imprinted maternally expressed transcript Homo sapiens 17-20 15013932-1 2004 Pimecrolimus (SDZ ASM 981, Elidel ) is an ascomycin macrolactam derivative and a cell-selective inhibitor of inflammatory cytokines specifically developed to treat inflammatory skin diseases. Sulfadiazine 14-17 H19 imprinted maternally expressed transcript Homo sapiens 18-21 15013932-1 2004 Pimecrolimus (SDZ ASM 981, Elidel ) is an ascomycin macrolactam derivative and a cell-selective inhibitor of inflammatory cytokines specifically developed to treat inflammatory skin diseases. immunomycin 42-51 H19 imprinted maternally expressed transcript Homo sapiens 18-21 12427740-6 2003 We asked if MeCP2 can deliver Lys(9) H3 methylation to the H19 gene, whose activity it represses. Lysine 30-33 H19 imprinted maternally expressed transcript Homo sapiens 59-62 12937131-5 2003 RA-ST contained a significantly higher percentage of strongly positive lining cells than OA-ST and N/JT-ST. H19 RNA was expressed in both Mphi and SFBs, as confirmed by RT-PCR in isolated RA Mphi and SFBs (n = 3). N-succinimidyl 8-((4'-fluorobenzyl)amino)suberate 147-151 H19 imprinted maternally expressed transcript Homo sapiens 108-111 12937131-5 2003 RA-ST contained a significantly higher percentage of strongly positive lining cells than OA-ST and N/JT-ST. H19 RNA was expressed in both Mphi and SFBs, as confirmed by RT-PCR in isolated RA Mphi and SFBs (n = 3). N-succinimidyl 8-((4'-fluorobenzyl)amino)suberate 200-204 H19 imprinted maternally expressed transcript Homo sapiens 108-111 12588801-0 2003 Loss of imprinting of IGF2 and H19 in osteosarcoma is accompanied by reciprocal methylation changes of a CTCF-binding site. ctcf 105-109 H19 imprinted maternally expressed transcript Homo sapiens 31-34 12588801-6 2003 Our data demonstrate that IGF2 LOI and H19 LOI are accompanied by reciprocal methylation changes at a critical CTCF-binding site. ctcf 111-115 H19 imprinted maternally expressed transcript Homo sapiens 39-42 14654216-7 2003 The DMR located upstream of the ovine H19 gene was found to be similarly organised as in humans and mice, with multiple CTCF binding sites. aspartylmethionylarginine 4-7 H19 imprinted maternally expressed transcript Homo sapiens 38-41 14654216-7 2003 The DMR located upstream of the ovine H19 gene was found to be similarly organised as in humans and mice, with multiple CTCF binding sites. ctcf 120-124 H19 imprinted maternally expressed transcript Homo sapiens 38-41 12419837-5 2002 But in anchorage-independent growth assays the H19-recombined cells formed more and larger colonies in soft-agar versus control cells. Agar 108-112 H19 imprinted maternally expressed transcript Homo sapiens 47-50 12619819-6 2002 In contrary, addition of ASM at a concentration of 20 microM to King"s B liquid medium significantly increased production of salicylic acid by isolate G309. king"s b liquid medium 64-86 H19 imprinted maternally expressed transcript Homo sapiens 25-28 12619819-6 2002 In contrary, addition of ASM at a concentration of 20 microM to King"s B liquid medium significantly increased production of salicylic acid by isolate G309. Salicylic Acid 125-139 H19 imprinted maternally expressed transcript Homo sapiens 25-28 14606933-1 2003 OBJECTIVE: To investigate the pharmacokinetics and tolerability of the new nonsteroid anti-inflammatory pimecrolimus (SDZ ASM 981, Elidel) after oral administration. pimecrolimus 104-116 H19 imprinted maternally expressed transcript Homo sapiens 122-125 14606933-1 2003 OBJECTIVE: To investigate the pharmacokinetics and tolerability of the new nonsteroid anti-inflammatory pimecrolimus (SDZ ASM 981, Elidel) after oral administration. Sulfadiazine 118-121 H19 imprinted maternally expressed transcript Homo sapiens 122-125 12619819-1 2002 Fluorescent pseudomonad isolates G309 and CW2, in combination with the resistance inducer acibenzolar-S-methyl (ASM), improved control of fungal and bacterial diseases on tomato plants. methyl radical 101-110 H19 imprinted maternally expressed transcript Homo sapiens 112-115 12234381-5 2002 In contrast, mild treatment of the cells with the methylation inhibitor 5-AzaC-2"-deoxycytidine (AzaC) on its own was able to reactivate H19. 5-azac-2"-deoxycytidine 72-95 H19 imprinted maternally expressed transcript Homo sapiens 137-140 12234381-5 2002 In contrast, mild treatment of the cells with the methylation inhibitor 5-AzaC-2"-deoxycytidine (AzaC) on its own was able to reactivate H19. 3,5-di-t-butyl-4-methylphenyl N-methylcarbamate 74-78 H19 imprinted maternally expressed transcript Homo sapiens 137-140 11597130-7 2001 Furthermore, it was demonstrated that H19 was reactivated and demethylated in the HepT1 cell line by 5-azaCytidine, in contrast to IGF2 P3, which was not demethylated or reactivated. Azacitidine 101-114 H19 imprinted maternally expressed transcript Homo sapiens 38-41 11889182-3 2002 We used PCR-based methylation analysis and bisulfite genomic sequencing to study the cytosine methylation status of the H19 promoter region in 16 normal adrenals and 30 pathological adrenocortical samples. Cytosine 85-93 H19 imprinted maternally expressed transcript Homo sapiens 120-123 11889182-5 2002 Bisulfite genomic sequencing revealed a significantly higher mean degree of methylation at each of 12 CpG sites of the H19 promoter in adrenocortical carcinomas than in normal adrenals (P < 0.01 for all sites) or adrenocortical adenomas (P < 0.01, except P < 0.05 for site 12 and P > 0.05 for site 11). hydrogen sulfite 0-9 H19 imprinted maternally expressed transcript Homo sapiens 119-122 11889182-10 2002 Treatment with a cytosine methylation inhibitor, 5-aza-2"-deoxycytidine, increased H19 RNA expression, whereas it decreased IGF-II mRNA accumulation dose- and time-dependently (both P < 0.005) and reduced cell proliferation to 10% in 7 d. Our results suggest that altered DNA methylation of the H19 promoter is involved in the abnormal expression of both H19 and IGF-II genes in human adrenocortical carcinomas. Decitabine 49-71 H19 imprinted maternally expressed transcript Homo sapiens 83-86 11889182-10 2002 Treatment with a cytosine methylation inhibitor, 5-aza-2"-deoxycytidine, increased H19 RNA expression, whereas it decreased IGF-II mRNA accumulation dose- and time-dependently (both P < 0.005) and reduced cell proliferation to 10% in 7 d. Our results suggest that altered DNA methylation of the H19 promoter is involved in the abnormal expression of both H19 and IGF-II genes in human adrenocortical carcinomas. Decitabine 49-71 H19 imprinted maternally expressed transcript Homo sapiens 298-301 11889182-10 2002 Treatment with a cytosine methylation inhibitor, 5-aza-2"-deoxycytidine, increased H19 RNA expression, whereas it decreased IGF-II mRNA accumulation dose- and time-dependently (both P < 0.005) and reduced cell proliferation to 10% in 7 d. Our results suggest that altered DNA methylation of the H19 promoter is involved in the abnormal expression of both H19 and IGF-II genes in human adrenocortical carcinomas. Decitabine 49-71 H19 imprinted maternally expressed transcript Homo sapiens 298-301 11298537-0 2001 First experience of topical SDZ ASM 981 in children with atopic dermatitis. Sulfadiazine 28-31 H19 imprinted maternally expressed transcript Homo sapiens 32-35 11298537-1 2001 BACKGROUND: SDZ ASM 981 is a selective inhibitor of inflammatory cytokine release under development for the topical treatment of atopic dermatitis. Sulfadiazine 12-15 H19 imprinted maternally expressed transcript Homo sapiens 16-19 11298537-2 2001 OBJECTIVES: This first paediatric study was designed to measure the systemic exposure to SDZ ASM 981 in young children with atopic dermatitis treated on extensive skin areas. Sulfadiazine 89-92 H19 imprinted maternally expressed transcript Homo sapiens 93-96 11298537-3 2001 METHODS: Children 1-4 years of age referred to a tertiary care centre for their atopic dermatitis were treated twice daily for 3 weeks with 1% SDZ ASM 981 cream. Sulfadiazine 143-146 H19 imprinted maternally expressed transcript Homo sapiens 147-150 11298537-4 2001 SDZ ASM 981 blood concentrations were measured on day 4 and 22 (last day) of treatment, and 1 week after the last application, using a radioimmunoassay with a limit of quantification of 0.5 ng mL(-1). Sulfadiazine 0-3 H19 imprinted maternally expressed transcript Homo sapiens 4-7 11298537-7 2001 Of the 63 SDZ ASM 981 blood concentrations measured, 63% were < 0.5 ng mL(-1); the maximum value observed was 1.8 ng mL-1. Sulfadiazine 10-13 H19 imprinted maternally expressed transcript Homo sapiens 14-17 11298537-11 2001 CONCLUSIONS: In these children 1-4 years of age, blood concentrations of SDZ ASM 981 during topical treatment with the 1% cream were consistently low even in the children with the most extensive areas treated (up to 69% of their BSA). Sulfadiazine 73-76 H19 imprinted maternally expressed transcript Homo sapiens 77-80 11260007-0 2001 The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study. immunomycin 16-25 H19 imprinted maternally expressed transcript Homo sapiens 41-44 11260007-0 2001 The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study. Sulfadiazine 37-40 H19 imprinted maternally expressed transcript Homo sapiens 41-44 11260007-1 2001 BACKGROUND: SDZ ASM 981 is a selective inhibitor of inflammatory cytokines released from T lymphocytes and mast cells, which has been developed for the treatment of inflammatory skin diseases. Sulfadiazine 12-15 H19 imprinted maternally expressed transcript Homo sapiens 16-19 11260007-2 2001 OBJECTIVES: In the present study, the atrophogenic potential of SDZ ASM 981 1% cream in humans was compared with that of medium and highly potent topical steroids, and vehicle. Sulfadiazine 64-67 H19 imprinted maternally expressed transcript Homo sapiens 68-71 11260007-6 2001 The difference in skin thickness (measured by ultrasound examination) between patients treated with SDZ ASM 981 1% cream and those receiving either of the two topical steroids was significant from day 8 onwards. Sulfadiazine 100-103 H19 imprinted maternally expressed transcript Homo sapiens 104-107 10792216-0 2000 Atopic dermatitis-like symptoms in hypomagnesaemic hairless rats are prevented and inhibited by systemic or topical SDZ ASM 981. Sulfadiazine 116-119 H19 imprinted maternally expressed transcript Homo sapiens 120-123 11120891-3 2001 LOI of IGF2 correlated strongly with biallelic hypermethylation of a core of five CpG sites in the insulator region of IGF2/H19, which is a known CTCF-binding element. ctcf 146-150 H19 imprinted maternally expressed transcript Homo sapiens 124-127 18034583-0 2000 SDZ ASM 981: a viewpoint by Jan D. Bos. Sulfadiazine 0-3 H19 imprinted maternally expressed transcript Homo sapiens 4-7 10792216-4 2000 The efficacy of the new ascomycin macrolactam derivative SDZ ASM 981 was tested in hypomagnesaemic rats by systemic or topical administration using prophylactic or therapeutic treatment regimens. immunomycin 24-33 H19 imprinted maternally expressed transcript Homo sapiens 61-64 10792216-4 2000 The efficacy of the new ascomycin macrolactam derivative SDZ ASM 981 was tested in hypomagnesaemic rats by systemic or topical administration using prophylactic or therapeutic treatment regimens. Sulfadiazine 57-60 H19 imprinted maternally expressed transcript Homo sapiens 61-64 10792216-7 2000 The same daily oral dose of SDZ ASM 981 administered before the onset of the rash proved to be an efficacious prophylactic treatment regimen to prevent signs. Sulfadiazine 28-31 H19 imprinted maternally expressed transcript Homo sapiens 32-35 10792216-8 2000 Topical treatment of the ears with 0.4% SDZ ASM 981 locally inhibited and prevented inflammatory changes in a therapeutic and prophylactic treatment regimen, respectively. Sulfadiazine 40-43 H19 imprinted maternally expressed transcript Homo sapiens 44-47 10792216-10 2000 The pharmacological activity of SDZ ASM 981 reported here corresponds well to its anti-inflammatory and antipruritic activity observed in atopic dermatitis patients, confirming the usefulness of this rat model in drug evaluations. Sulfadiazine 32-35 H19 imprinted maternally expressed transcript Homo sapiens 36-39 11060661-3 2000 Several compounds are being developed with SDZ ASM 981 being at the most advanced stage. Sulfadiazine 43-46 H19 imprinted maternally expressed transcript Homo sapiens 47-50 11060661-5 2000 Topical application of SDZ ASM 981 was shown to be effective in atopic dermatitis (AD), allergic contact dermatitis and also in psoriasis under semi-occlusive conditions. Sulfadiazine 23-26 H19 imprinted maternally expressed transcript Homo sapiens 27-30 11060661-6 2000 In patients with AD, SDZ ASM 981 cream led to consistently low systemic exposure even when applied on large areas of skin. Sulfadiazine 21-24 H19 imprinted maternally expressed transcript Homo sapiens 25-28 11060661-7 2000 SDZ ASM 981 overcomes the drawbacks of current topical therapies of inflammatory skin diseases as its safety profile is better than that of topical corticosteroids. Sulfadiazine 0-3 H19 imprinted maternally expressed transcript Homo sapiens 4-7 10442637-0 1999 Steroid hormones modulate H19 gene expression in both mammary gland and uterus. Steroids 0-16 H19 imprinted maternally expressed transcript Homo sapiens 26-29 10468798-0 1999 A novel anti-inflammatory drug, SDZ ASM 981, for the treatment of skin diseases: in vitro pharmacology. Sulfadiazine 32-35 H19 imprinted maternally expressed transcript Homo sapiens 36-39 10442637-3 1999 To determine the mode of steroid action, we have detected levels of H19 RNA synthesis during mammary gland development by in situ hybridization (ISH): two peaks of H19 transcription occur during puberty and pregnancy. Steroids 25-32 H19 imprinted maternally expressed transcript Homo sapiens 68-71 10442637-3 1999 To determine the mode of steroid action, we have detected levels of H19 RNA synthesis during mammary gland development by in situ hybridization (ISH): two peaks of H19 transcription occur during puberty and pregnancy. Steroids 25-32 H19 imprinted maternally expressed transcript Homo sapiens 164-167 10442637-15 1999 We have thus demonstrated that H19 gene expression is controlled by steroid hormones; furthermore, this gene is highly expressed in hormone-sensitive organs when the hormonal stimulation is accompanied with a morphological repair. Steroids 68-84 H19 imprinted maternally expressed transcript Homo sapiens 31-34 10333615-5 1999 Similarly new immunomodulatory therapies show great promise for the lymphocyte-associated alopecias and include a new generation of macrolide immunosuppressives (tacrolimus, SDZ ASM 981, and SDZ 281-240), some of which appear to have good transcutaneous absorption. Macrolides 132-141 H19 imprinted maternally expressed transcript Homo sapiens 178-181 10428315-2 1999 DESIGN: In situ hybridization for H19 RNA using S-labeled and digoxigenin-labeled probes was performed on paraffin sections of ovarian surface epithelial tumors. Paraffin 106-114 H19 imprinted maternally expressed transcript Homo sapiens 34-37 9618710-6 1998 Although ASM is known to contract in response to acetylcholine via muscarinic M3 receptors and this contractile response is augmented during AHR, no alteration in muscarinic receptor density in ASM has been demonstrated in various AHR models. Acetylcholine 49-62 H19 imprinted maternally expressed transcript Homo sapiens 9-12 9859912-3 1998 SDZ ASM 981 is the most advanced ascomycin derivative under development. Sulfadiazine 0-3 H19 imprinted maternally expressed transcript Homo sapiens 4-7 9859912-3 1998 SDZ ASM 981 is the most advanced ascomycin derivative under development. immunomycin 33-42 H19 imprinted maternally expressed transcript Homo sapiens 4-7 9859912-5 1998 Topical application of SDZ ASM 981 has been shown to be effective in atopic dermatitis (AD) and allergic contact dermatitis. Sulfadiazine 23-26 H19 imprinted maternally expressed transcript Homo sapiens 27-30 9859912-7 1998 SDZ ASM 981 holds promise in overcoming the drawbacks of topical corticosteroids and studies are ongoing to further investigate its efficacy and safety in the treatment of inflammatory skin diseases. Sulfadiazine 0-3 H19 imprinted maternally expressed transcript Homo sapiens 4-7 9681343-0 1998 Effectiveness of the ascomycin macrolactam SDZ ASM 981 in the topical treatment of atopic dermatitis. immunomycin 21-30 H19 imprinted maternally expressed transcript Homo sapiens 47-50 9681343-0 1998 Effectiveness of the ascomycin macrolactam SDZ ASM 981 in the topical treatment of atopic dermatitis. Sulfadiazine 43-46 H19 imprinted maternally expressed transcript Homo sapiens 47-50 9681343-1 1998 OBJECTIVE: To compare the safety and efficacy of 1% SDZ ASM 981 cream and a matching placebo cream in the treatment of patients with moderate atopic dermatitis. Sulfadiazine 52-55 H19 imprinted maternally expressed transcript Homo sapiens 56-59 9681343-5 1998 INTERVENTION: Topical 1% SDZ ASM 981 cream was applied twice daily (n=16) or once daily (n=18) and compared with a corresponding placebo cream base. Sulfadiazine 25-28 H19 imprinted maternally expressed transcript Homo sapiens 29-32 9681343-12 1998 Within 3 weeks of topical therapy with 1% SDZ ASM 981 cream twice daily, a mean reduction of 71.9% in the ADSI score was observed at the actively treated test sites compared with a mean reduction of 10.3% at the placebo-treated test sites (P<.001). Sulfadiazine 42-45 H19 imprinted maternally expressed transcript Homo sapiens 46-49 9681343-16 1998 CONCLUSIONS: Treatment with 1% SDZ ASM 981 cream was well tolerated. Sulfadiazine 31-34 H19 imprinted maternally expressed transcript Homo sapiens 35-38 9681343-17 1998 Twice-daily application of 1% SDZ ASM 981 cream was significantly more effective than use of the corresponding placebo and more effective than once-daily treatment. Sulfadiazine 30-33 H19 imprinted maternally expressed transcript Homo sapiens 34-37 9681343-18 1998 The new macrolactam ascomycin derivative SDZ ASM 981 is a promising agent for the treatment of patients with atopic dermatitis. immunomycin 20-29 H19 imprinted maternally expressed transcript Homo sapiens 45-48 9681343-18 1998 The new macrolactam ascomycin derivative SDZ ASM 981 is a promising agent for the treatment of patients with atopic dermatitis. Sulfadiazine 41-44 H19 imprinted maternally expressed transcript Homo sapiens 45-48 9990361-0 1998 The novel ascomycin derivative SDZ ASM 981 is effective for psoriasis when used topically under occlusion. immunomycin 10-19 H19 imprinted maternally expressed transcript Homo sapiens 35-38 9990361-0 1998 The novel ascomycin derivative SDZ ASM 981 is effective for psoriasis when used topically under occlusion. Sulfadiazine 31-34 H19 imprinted maternally expressed transcript Homo sapiens 35-38 9990361-1 1998 Topical SDZ ASM 981 has been found to be highly effective in preclinical models of T-cell-mediated skin disease. Sulfadiazine 8-11 H19 imprinted maternally expressed transcript Homo sapiens 12-15 9990361-3 1998 It has been hypothesized that SDZ ASM 981 may prove to be an effective treatment for chronic plaque psoriasis. Sulfadiazine 30-33 H19 imprinted maternally expressed transcript Homo sapiens 34-37 9990361-4 1998 Therefore, the study objective was to determine the efficacy, tolerability and safety of the new topical macrolactam, SDZ ASM 981, for chronic plaque psoriasis. Sulfadiazine 118-121 H19 imprinted maternally expressed transcript Homo sapiens 122-125 9990361-7 1998 The results of the study showed that, after 2 weeks of treatment, total scores described by 92% for clobetasol, by 82% for 1 SDZ ASM 981, by 63% for 0.3% SDZ ASM 981 and by 18% for the ointment base (placebo). Sulfadiazine 154-157 H19 imprinted maternally expressed transcript Homo sapiens 158-161 9990361-9 1998 We conclude from our results that the new macrolactam SDZ ASM 981 (1%) is similar to clobetasol-17-propionate (0.05%) in plaque-type psoriasis when applied topically under occlusion for 2 weeks using the microplaque assay. Sulfadiazine 54-57 H19 imprinted maternally expressed transcript Homo sapiens 58-61 9720909-0 1998 The effect of retinoic acid on the activation of the human H19 promoter by a 3" downstream region. Tretinoin 14-27 H19 imprinted maternally expressed transcript Homo sapiens 59-62 9720909-5 1998 Moreover, the activation of the H19 promoter by retinoic acid in cells derived from human testicular germ cell tumors is dependent upon the 3" downstream region. Tretinoin 48-61 H19 imprinted maternally expressed transcript Homo sapiens 32-35 9720909-6 1998 The possibility that the action of retinoic acid on the H19 promoter is an indirect one and involves a member of the AP2 transcription factor family is discussed. Tretinoin 35-48 H19 imprinted maternally expressed transcript Homo sapiens 56-59 9620557-4 1998 Moreover, a HeLa clone stably transfected with a temperature sensitive (ts) 143 Ala p53 mutant exhibited temperature-dependent regulation of H19 expression. Alanine 80-83 H19 imprinted maternally expressed transcript Homo sapiens 141-144 9618710-8 1998 In fact, recent investigations demonstrated increases in the levels of GTP binding protein, Ca2+ mobilization and inositol 1,4,5-trisphosphate generation and so on in hyperresponsive ASM. Guanosine Triphosphate 71-74 H19 imprinted maternally expressed transcript Homo sapiens 183-186 9618710-8 1998 In fact, recent investigations demonstrated increases in the levels of GTP binding protein, Ca2+ mobilization and inositol 1,4,5-trisphosphate generation and so on in hyperresponsive ASM. Inositol 1,4,5-Trisphosphate 114-142 H19 imprinted maternally expressed transcript Homo sapiens 183-186 9269541-24 1997 Dialysis of the alpha o common antisense oligonucleotides (ASm) but not the alpha i3 AS significantly diminished the inhibitory effect of SRIF on the Ca2+ current. Oligonucleotides 41-57 H19 imprinted maternally expressed transcript Homo sapiens 59-62 9075580-9 1996 The reactivity with one monoclonal antibody, H19, was abrogated by the mutations 61Tyr-->Gly and 61Tyr-->Ala. Glycine 92-95 H19 imprinted maternally expressed transcript Homo sapiens 45-48 9177379-8 1997 In cultured adrenocortical cells, ACTH and dibutyryl cAMP treatment slightly reduced the predominant 1.7-kilobase (kb) transcript of p57KIP2 gene, but induced a 2.5-kb transcript with a simultaneous increase in H19 RNA expression. Cyclic AMP 53-57 H19 imprinted maternally expressed transcript Homo sapiens 211-214 9208812-8 1997 METHODS: Using in situ hybridisation with a [35S] labelled probe, H19 mRNA was detected in paraffin wax sections of fetal tissues from the first and second trimesters of pregnancy and of a large array of human adult and childhood tumours arising from these tissues. Sulfur-35 45-48 H19 imprinted maternally expressed transcript Homo sapiens 66-69 9208812-8 1997 METHODS: Using in situ hybridisation with a [35S] labelled probe, H19 mRNA was detected in paraffin wax sections of fetal tissues from the first and second trimesters of pregnancy and of a large array of human adult and childhood tumours arising from these tissues. Paraffin 91-103 H19 imprinted maternally expressed transcript Homo sapiens 66-69 9310237-4 1997 Methylation of particular cytosine residues of H19 correlates with inhibition of expression, which has not been studied in TGCTs thus far. Cytosine 26-34 H19 imprinted maternally expressed transcript Homo sapiens 47-50 8842727-7 1996 5-aza-2"-deoxycytidine (aza-C) increases H19 expression in RD RMS cells but does not activate KIP2 expression. Decitabine 0-22 H19 imprinted maternally expressed transcript Homo sapiens 41-44 8842727-7 1996 5-aza-2"-deoxycytidine (aza-C) increases H19 expression in RD RMS cells but does not activate KIP2 expression. Decitabine 24-29 H19 imprinted maternally expressed transcript Homo sapiens 41-44 8636375-11 1996 H19 imprinting was maintained in all 18 informative fresh-frozen and paraffin-embedded formalin-fixed samples. Paraffin 69-77 H19 imprinted maternally expressed transcript Homo sapiens 0-3 8636375-11 1996 H19 imprinting was maintained in all 18 informative fresh-frozen and paraffin-embedded formalin-fixed samples. Formaldehyde 87-95 H19 imprinted maternally expressed transcript Homo sapiens 0-3 9028733-5 1997 We examined the expression of H19 in the endometrium and ovary during the menstrual cycle by in situ hybridization applied to paraffin sections of human endometrium and ovaries at different stages of differentiation. Paraffin 126-134 H19 imprinted maternally expressed transcript Homo sapiens 30-33 9025899-4 1996 We studied the expression of the H19 gene by in-situ hybridization performed on paraffin sections of the kidney. Paraffin 80-88 H19 imprinted maternally expressed transcript Homo sapiens 33-36 9075580-9 1996 The reactivity with one monoclonal antibody, H19, was abrogated by the mutations 61Tyr-->Gly and 61Tyr-->Ala. Alanine 111-114 H19 imprinted maternally expressed transcript Homo sapiens 45-48 8021956-6 1994 To determine if there was heterozygosity of the Alu I and Apa I restriction site polymorphism in the H19 and IGF2 genes, respectively, DNA was isolated from cells of the peripheral blood of these patients, then subjected to polymerase chain reaction (PCR) amplification, restriction enzyme digestion, and electrophoresis in agarose gels. Sepharose 324-331 H19 imprinted maternally expressed transcript Homo sapiens 101-104 7855987-6 1995 METHODS: In situ hybridization for H19 mRNA on paraffin sections of bladder carcinoma in different histologic grades. Paraffin 47-55 H19 imprinted maternally expressed transcript Homo sapiens 35-38 7512497-6 1994 Staurosporine, a protein kinase-C inhibitor, increased H19 and IGF-II RNA to the same extent as did ACTH. Staurosporine 0-13 H19 imprinted maternally expressed transcript Homo sapiens 55-58 8050357-6 1994 Igf2, H19 and Igf2r were all appropriately expressed in the PGES derived cells following induction of differentiation in vitro with all-trans retinoic acid or DMSO, when compared with control (D3) and androgenetic ES cells (AGES). pges 60-64 H19 imprinted maternally expressed transcript Homo sapiens 6-9 7512497-7 1994 The protein kinase-C activator 12-O-tetradecanoyl phorbol-13-acetate and cytokines, tumor necrosis factor-alpha and interferon-gamma, inhibited H19 and IGF-II RNA accumulation. Tetradecanoylphorbol Acetate 31-68 H19 imprinted maternally expressed transcript Homo sapiens 144-147 34934057-3 2021 H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). Phenobarbital 118-125 H19 imprinted maternally expressed transcript Homo sapiens 0-3 1395777-1 1992 To visualize ASM contraction in vitro, we measured changes in cross-sectional area and inner circumference of isolated porcine and human bronchi in response to acetylcholine or carbamylcholine chloride (Carbachol) using high-frequency ultrasound. Carbachol 177-201 H19 imprinted maternally expressed transcript Homo sapiens 13-16 33824697-2 2021 NADPH oxidase 4- (NOX4-) mediated reactive oxygen species (ROS) production plays a crucial role in cell differentiation and extracellular matrix (ECM) synthesis in ASM remodeling. Reactive Oxygen Species 34-57 H19 imprinted maternally expressed transcript Homo sapiens 164-167 34815764-0 2022 Long non-coding RNA H19 mediates N-acetyltransferase 1 gene methylation in the development of tamoxifen resistance in breast cancer. Tamoxifen 94-103 H19 imprinted maternally expressed transcript Homo sapiens 20-23 34815764-2 2022 H19 lncRNA has been demonstrated to be an estrogen-inducible gene, the expression of which is significantly increased in tamoxifen (TAM)-resistant MCF-7 breast cancer cells. Tamoxifen 121-130 H19 imprinted maternally expressed transcript Homo sapiens 0-3 34815764-2 2022 H19 lncRNA has been demonstrated to be an estrogen-inducible gene, the expression of which is significantly increased in tamoxifen (TAM)-resistant MCF-7 breast cancer cells. Tamoxifen 132-135 H19 imprinted maternally expressed transcript Homo sapiens 0-3 34815764-3 2022 The aim of the present study was to investigate the role and molecular mechanism of lncRNA H19 in the development of TAM resistance. Tamoxifen 117-120 H19 imprinted maternally expressed transcript Homo sapiens 91-94 34815764-6 2022 Furthermore, when H19 was knocked down in the MCF-7R cells, the sensitivity to 4-hydroxytamoxifen was markedly restored. afimoxifene 79-97 H19 imprinted maternally expressed transcript Homo sapiens 18-21 34815764-7 2022 The results further demonstrated that N-acetyltransferase 1 (NAT1) may serve an important role in TAM-resistant cells, as NAT1 expression was notably downregulated in the MCF-7R cells but significantly elevated following the knockdown of H19. Tamoxifen 98-101 H19 imprinted maternally expressed transcript Homo sapiens 238-241 34815764-8 2022 In addition, lower expression of NAT1 and higher expression of H19 were indicated to be associated with poor prognosis in patients with breast cancer treated with TAM. Tamoxifen 163-166 H19 imprinted maternally expressed transcript Homo sapiens 63-66 34815764-9 2022 The results of bisulfite genomic sequencing PCR analysis indicated that the methylation rate of NAT1 in MCF-7R cells was significantly higher compared with that in MCF-7 cells, while the methylation rate of NAT1 in TAM-resistant cells transfected with small interfering RNA against H19 was significantly lower than that in the corresponding untransfected cells. Tamoxifen 215-218 H19 imprinted maternally expressed transcript Homo sapiens 282-285 34278583-1 2022 Diacylglycerol kinase (DGK), a lipid kinase, catalyzes the conversion of diacylglycerol (DAG) to phosphatidic acid, thereby terminating DAG-mediated signaling by Gq-coupled receptors that regulate contraction of airway smooth muscle (ASM). Diglycerides 73-87 H19 imprinted maternally expressed transcript Homo sapiens 234-237 34278583-1 2022 Diacylglycerol kinase (DGK), a lipid kinase, catalyzes the conversion of diacylglycerol (DAG) to phosphatidic acid, thereby terminating DAG-mediated signaling by Gq-coupled receptors that regulate contraction of airway smooth muscle (ASM). Diglycerides 89-92 H19 imprinted maternally expressed transcript Homo sapiens 234-237 34278583-1 2022 Diacylglycerol kinase (DGK), a lipid kinase, catalyzes the conversion of diacylglycerol (DAG) to phosphatidic acid, thereby terminating DAG-mediated signaling by Gq-coupled receptors that regulate contraction of airway smooth muscle (ASM). Phosphatidic Acids 97-114 H19 imprinted maternally expressed transcript Homo sapiens 234-237 34278583-1 2022 Diacylglycerol kinase (DGK), a lipid kinase, catalyzes the conversion of diacylglycerol (DAG) to phosphatidic acid, thereby terminating DAG-mediated signaling by Gq-coupled receptors that regulate contraction of airway smooth muscle (ASM). Diglycerides 136-139 H19 imprinted maternally expressed transcript Homo sapiens 234-237 34278583-6 2022 Furthermore, inhibition of DGK resulted in induction of cyclooxygenase (COX) and generation of prostaglandin E2 (PGE2 ) with concomitant activation of Gs-cAMP-PKA signaling in ASM cells in an autocrine/paracrine fashion. Cyclic AMP 154-158 H19 imprinted maternally expressed transcript Homo sapiens 176-179 34278583-8 2022 Finally, DGK inhibition-mediated attenuation of contractile agonist-induced phosphorylation of myosin light chain 20 (MLC-20), a marker of ASM contraction, involves COX-mediated cAMP production and PKA activation in ASM cells. Cyclic AMP 178-182 H19 imprinted maternally expressed transcript Homo sapiens 139-142 34992498-12 2021 lncRNA H19 repressed proliferation and inflammation, which were reduced by the miR-766-3p. mir-766 79-86 H19 imprinted maternally expressed transcript Homo sapiens 7-10 33824697-2 2021 NADPH oxidase 4- (NOX4-) mediated reactive oxygen species (ROS) production plays a crucial role in cell differentiation and extracellular matrix (ECM) synthesis in ASM remodeling. Reactive Oxygen Species 59-62 H19 imprinted maternally expressed transcript Homo sapiens 164-167 34480309-9 2022 Compared with participants in quartile 1, those in quartile 2 of urinary mono-n-butyl phthalate (MnBP) and quartile 4 of urinary monobenzyl phthalate (MBzP) had decreased ASM/BMI. monobutyl phthalate 97-101 H19 imprinted maternally expressed transcript Homo sapiens 171-174 34480309-9 2022 Compared with participants in quartile 1, those in quartile 2 of urinary mono-n-butyl phthalate (MnBP) and quartile 4 of urinary monobenzyl phthalate (MBzP) had decreased ASM/BMI. mono-benzyl phthalate 129-149 H19 imprinted maternally expressed transcript Homo sapiens 171-174 34480309-9 2022 Compared with participants in quartile 1, those in quartile 2 of urinary mono-n-butyl phthalate (MnBP) and quartile 4 of urinary monobenzyl phthalate (MBzP) had decreased ASM/BMI. mono-benzyl phthalate 151-155 H19 imprinted maternally expressed transcript Homo sapiens 171-174 34815764-10 2022 Therefore, the present study suggests that the H19 gene regulates NAT1 expression in TAM-resistant cells via the mediation of NAT1 promoter methylation. Tamoxifen 85-88 H19 imprinted maternally expressed transcript Homo sapiens 47-50 34934057-3 2021 H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown). Phenobarbital 118-125 H19 imprinted maternally expressed transcript Homo sapiens 137-140 34934057-4 2021 It contributes to treatment resistance, with the knockdown of H19 re-sensitizing PCa to ADT. adt 88-91 H19 imprinted maternally expressed transcript Homo sapiens 62-65 34934057-10 2021 Our clinical data identify H19 as a candidate diagnostic marker and predictive marker of NEPC with elevated H19 levels associated with an increased probability of biochemical recurrence and metastatic disease in patients receiving ADT. adt 231-234 H19 imprinted maternally expressed transcript Homo sapiens 108-111 34612067-7 2021 These findings suggest that the melatonin MT2 receptor is expressed in ASM, and modulates airway smooth muscle tone via reduced cAMP production and increased (Ca2+)i. Cyclic AMP 128-132 H19 imprinted maternally expressed transcript Homo sapiens 71-74 34293268-12 2021 Finally, DGK inhibition or treatment with DAG analog resulted in attenuation of activation of PLC in human ASM cells. Diglycerides 42-45 H19 imprinted maternally expressed transcript Homo sapiens 107-110 34293268-13 2021 Our findings suggest that DGK inhibition perturbed the DAG:PA ratio resulting in inhibition of Gq-PLC activation in a negative feedback manner, resulting in protection against ASM contraction. Diglycerides 55-58 H19 imprinted maternally expressed transcript Homo sapiens 176-179 34251961-14 2021 Moreover, miR-30b-5p overexpression facilitated the expression of p-PI3K and p-AKT in PDGF-stimulated ASM cells. mir-30b-5p 10-20 H19 imprinted maternally expressed transcript Homo sapiens 102-105 34288826-11 2021 miR-106b-5p is predicted to be a target of H19. mir-106b-5p 0-11 H19 imprinted maternally expressed transcript Homo sapiens 43-46 34656948-12 2021 The correlation between DXA-measured ASM and predicted ASM by the present equation was not significantly different from the correlation between DXA-measured ASM and BIA-measured ASM. bia 165-168 H19 imprinted maternally expressed transcript Homo sapiens 178-181 34784434-7 2021 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin 15-17 H19 imprinted maternally expressed transcript Homo sapiens 92-95 34784434-7 2021 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin 29-31 H19 imprinted maternally expressed transcript Homo sapiens 92-95 34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 44-46 H19 imprinted maternally expressed transcript Homo sapiens 19-22 34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 48-52 H19 imprinted maternally expressed transcript Homo sapiens 19-22 34609065-6 2021 Agreement analysis was performed to cross-validate ASM measurements by BIA and DXA. bia 71-74 H19 imprinted maternally expressed transcript Homo sapiens 51-54 34726962-3 2022 The administration of the deacetylase inhibitors (DACi) panobinostat, trichostatin A and SAHA affected the cell viability of H295R monolayer and spheroids and induced the over-expression of H19 and autophagy transcripts. Panobinostat 56-68 H19 imprinted maternally expressed transcript Homo sapiens 190-193 34726962-3 2022 The administration of the deacetylase inhibitors (DACi) panobinostat, trichostatin A and SAHA affected the cell viability of H295R monolayer and spheroids and induced the over-expression of H19 and autophagy transcripts. trichostatin A 70-84 H19 imprinted maternally expressed transcript Homo sapiens 190-193 34726962-5 2022 Instead, H19 knock down was able to impede the ability of DACi to modulate the protein level of the autophagy markers. daci 58-62 H19 imprinted maternally expressed transcript Homo sapiens 9-12 34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 38-51 H19 imprinted maternally expressed transcript Homo sapiens 320-323 34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 53-55 H19 imprinted maternally expressed transcript Homo sapiens 320-323 34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Vitamin A 82-91 H19 imprinted maternally expressed transcript Homo sapiens 320-323 34436746-0 2021 Silencing of H19 alleviates oxygen-glucose deprivation/reoxygenation-triggered injury through the regulation of the miR-1306-5p/BCL2L13 axis. Oxygen 28-34 H19 imprinted maternally expressed transcript Homo sapiens 13-16 34768177-7 2021 Valproic acid was the most-prescribed ASM (more than 30%), and levetiracetam has replaced phenytoin as the second choice since 2015. Valproic Acid 0-13 H19 imprinted maternally expressed transcript Homo sapiens 38-41 34549600-4 2021 Previously, we demonstrated that 6-shogaol (6S), the primary bioactive component of ginger, relaxes human airway smooth muscle (hASM) likely by inhibition of phosphodiesterases (PDEs) in the b-adrenergic (cyclic nucleotide PDEs) and muscarinic (phospholipase C, PLC) receptor pathways. shogaol 33-42 H19 imprinted maternally expressed transcript Homo sapiens 128-132 34355539-10 2021 Admission to the NICU may lower the odds, and ASySs (convulsive or electrographic) and EAs on cEEG significantly increase the odds of long-term ASM use. CHEMBL4167713 87-90 H19 imprinted maternally expressed transcript Homo sapiens 144-147 34517264-0 2021 Combination of curcumin with N-n-butyl haloperidol iodide inhibits hepatocellular carcinoma malignant proliferation by downregulating enhancer of zeste homolog 2 (EZH2) - lncRNA H19 to silence Wnt/beta-catenin signaling. Curcumin 15-23 H19 imprinted maternally expressed transcript Homo sapiens 178-181 34420817-4 2021 Patients in the lowest ASM/body mass index (BMI) or GS/BMI tertile were older and had lower HDL cholesterol, and eGFR, but higher BMI, waist circumference (WC), HOMA-IR, and C-reactive protein than those in the highest tertile. Cholesterol 96-107 H19 imprinted maternally expressed transcript Homo sapiens 23-26 34746584-1 2021 With the aim of upgrading the power conversion efficiency of organic solar cells (OSCs), four novel non-fullerene, A1-A2-D-A2-A1-type small molecules were designed that are derivatives of a recently synthesized molecule SBDT-BDD reported for its efficient properties in all-small-molecule OSCs (ASM-OSCs). Fullerenes 104-113 H19 imprinted maternally expressed transcript Homo sapiens 295-298 34746584-1 2021 With the aim of upgrading the power conversion efficiency of organic solar cells (OSCs), four novel non-fullerene, A1-A2-D-A2-A1-type small molecules were designed that are derivatives of a recently synthesized molecule SBDT-BDD reported for its efficient properties in all-small-molecule OSCs (ASM-OSCs). sbdt-bdd 220-228 H19 imprinted maternally expressed transcript Homo sapiens 295-298 34592982-0 2021 Quercetin promotes bone marrow mesenchymal stem cell proliferation and osteogenic differentiation through the H19/miR-625-5p axis to activate the Wnt/beta-catenin pathway. Quercetin 0-9 H19 imprinted maternally expressed transcript Homo sapiens 110-113 34592982-6 2021 Moreover, quercetin increased H19 expression, while the effect of quercetin on BMSCs was reversed by silencing H19 expression. Quercetin 10-19 H19 imprinted maternally expressed transcript Homo sapiens 30-33 34592982-6 2021 Moreover, quercetin increased H19 expression, while the effect of quercetin on BMSCs was reversed by silencing H19 expression. Quercetin 10-19 H19 imprinted maternally expressed transcript Homo sapiens 111-114 34592982-6 2021 Moreover, quercetin increased H19 expression, while the effect of quercetin on BMSCs was reversed by silencing H19 expression. Quercetin 66-75 H19 imprinted maternally expressed transcript Homo sapiens 111-114 34592982-7 2021 Additionally, miR-625-5p, interacted with H19, was downregulated during quercetin-induced BMSC osteogenic differentiation, which negatively correlated with H19 expression. Quercetin 72-81 H19 imprinted maternally expressed transcript Homo sapiens 42-45 34592982-7 2021 Additionally, miR-625-5p, interacted with H19, was downregulated during quercetin-induced BMSC osteogenic differentiation, which negatively correlated with H19 expression. Quercetin 72-81 H19 imprinted maternally expressed transcript Homo sapiens 156-159 34592982-10 2021 Upregulation or downregulation of miR-625-5p or H19 expression, respectively, inhibited beta-catenin protein level in quercetin treated-BMSCs. Quercetin 118-127 H19 imprinted maternally expressed transcript Homo sapiens 48-51 34592982-12 2021 Quercetin activates the Wnt/beta-catenin pathway and promotes BMSC osteogenic differentiation via the H19/miR-625-5p axis. Quercetin 0-9 H19 imprinted maternally expressed transcript Homo sapiens 102-105 34355539-10 2021 Admission to the NICU may lower the odds, and ASySs (convulsive or electrographic) and EAs on cEEG significantly increase the odds of long-term ASM use. ceeg 94-98 H19 imprinted maternally expressed transcript Homo sapiens 144-147 34251499-5 2021 In the study, we hypothesized that the functional lncRNA H19 SNP(s) might impact H19 expression and, thus, prognosis of TACE-treated HCC patients. Chlorotrianisene 120-124 H19 imprinted maternally expressed transcript Homo sapiens 81-84 34342165-7 2022 Spearman correlation, multiple regression analyses as well as receiver-operating characteristic (ROC) curve analysis were used to explore the correlation between ASM/height2 , BMD and bone metabolism markers RESULTS: Spearman correlation analysis showed that ASM/height2 had a positive correlation with serum calcium and BMD (r=0.209-0.404, P<0.01). Calcium 309-316 H19 imprinted maternally expressed transcript Homo sapiens 162-165 34251499-6 2021 We found that the H19 rs3741219 SNP was significantly associated with OS of HCC patients received TACE. Chlorotrianisene 98-102 H19 imprinted maternally expressed transcript Homo sapiens 18-21 34251499-11 2021 Knock-down of lncRNA H19 significantly promoted the anti-viability efficiency of oxaliplatin (the main chemotherapy drug used in TACE) to HCC cells. Oxaliplatin 81-92 H19 imprinted maternally expressed transcript Homo sapiens 21-24 34251499-11 2021 Knock-down of lncRNA H19 significantly promoted the anti-viability efficiency of oxaliplatin (the main chemotherapy drug used in TACE) to HCC cells. Chlorotrianisene 129-133 H19 imprinted maternally expressed transcript Homo sapiens 21-24 34291893-1 2021 In this work, three small molecular donors (SMDs) S35, S35-1Si, and S35-2Si, with 3,5-difluorophenyl-substituted benzodithiophene as the central 2-dimensional unit to combine different numbers of siloxane-terminated side chain, were synthesized for all-small-molecule organic solar cells (ASM-OSCs). 3,5-difluorophenyl-substituted benzodithiophene 82-129 H19 imprinted maternally expressed transcript Homo sapiens 289-292 34291893-8 2021 Our results suggest that the siloxane-terminated side chain is promising to regulate crystalline ability of a SMD, paving a way for high performance ASM-OSCs. Siloxanes 29-37 H19 imprinted maternally expressed transcript Homo sapiens 149-152 34288135-7 2021 Greater first trimester intake of omega-6 polyunsaturated fat (effect per 1% of calories at the expense of carbohydrates) was associated with lower DNA methylation of IGF2-DMR (-1.2%; 95% confidence interval (CI): -2.2%, -0.2%) and higher DNA methylation at H19-DMR (0.8%; 95% CI: 0.3%, 1.3%). omega-6 polyunsaturated fat 34-61 H19 imprinted maternally expressed transcript Homo sapiens 258-261 34288135-7 2021 Greater first trimester intake of omega-6 polyunsaturated fat (effect per 1% of calories at the expense of carbohydrates) was associated with lower DNA methylation of IGF2-DMR (-1.2%; 95% confidence interval (CI): -2.2%, -0.2%) and higher DNA methylation at H19-DMR (0.8%; 95% CI: 0.3%, 1.3%). Carbohydrates 107-120 H19 imprinted maternally expressed transcript Homo sapiens 258-261 34288135-8 2021 On the other hand, greater first trimester intake of omega-3 polyunsaturated fat was associated with lower DNA methylation of the H19-DMR (-4.3%; 95% CI: -7.9%, -0.8%). omega-3 polyunsaturated fat 53-80 H19 imprinted maternally expressed transcript Homo sapiens 130-133 34288135-10 2021 Our findings suggest that early prenatal fat intake (omega-3, omega-6, and saturated fatty acids) may influence DNA methylation at the IGF2 and H19 locus, which could impact fetal development and long-term health. omega-3, omega-6, and saturated fatty acids 53-96 H19 imprinted maternally expressed transcript Homo sapiens 144-147 34342165-7 2022 Spearman correlation, multiple regression analyses as well as receiver-operating characteristic (ROC) curve analysis were used to explore the correlation between ASM/height2 , BMD and bone metabolism markers RESULTS: Spearman correlation analysis showed that ASM/height2 had a positive correlation with serum calcium and BMD (r=0.209-0.404, P<0.01). Calcium 309-316 H19 imprinted maternally expressed transcript Homo sapiens 259-262 34393833-1 2021 Previously, we reported that in airway smooth muscle (ASM), the cytosolic Ca2+ ((Ca2+) cyt ) and force response induced by acetyl choline (ACh) are increased by exposure to the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha). Acetylcholine 123-137 H19 imprinted maternally expressed transcript Homo sapiens 54-57 34393833-1 2021 Previously, we reported that in airway smooth muscle (ASM), the cytosolic Ca2+ ((Ca2+) cyt ) and force response induced by acetyl choline (ACh) are increased by exposure to the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha). Acetylcholine 139-142 H19 imprinted maternally expressed transcript Homo sapiens 54-57 34197709-2 2021 For example, neurotransmitters (e.g., histamine) trigger calcium signals that induce actomyosin-regulated contraction of airway smooth muscle (ASM); the resulting cell shortening causes airway narrowing, the excess of which can cause asthma. Histamine 38-47 H19 imprinted maternally expressed transcript Homo sapiens 143-146 34324543-11 2021 ASM senescence may enhance fibrosis in a feed forward loop promoting remodeling and altered calcium storage and buffering. Calcium 92-99 H19 imprinted maternally expressed transcript Homo sapiens 0-3 34320092-0 2021 Retraction notice for: "Schizandrin A exerts anti-tumor effects on A375 cells by down-regulating H19" (Braz J Med Biol Res (2019) 52(10): e8385). schizandrin A 24-37 H19 imprinted maternally expressed transcript Homo sapiens 97-101 34197709-2 2021 For example, neurotransmitters (e.g., histamine) trigger calcium signals that induce actomyosin-regulated contraction of airway smooth muscle (ASM); the resulting cell shortening causes airway narrowing, the excess of which can cause asthma. Calcium 57-64 H19 imprinted maternally expressed transcript Homo sapiens 143-146 34909646-5 2021 Results: After a 60 min-challenge with CM 1:10 v/v and fat/lactose-free CM 1:10 v/v, ASM significantly (P < 0.05) increased compared to control (+67.04 +- 17.08% and +77.91 +- 1.34%, respectively), a condition that remained stable for 150 min post-treatment, whereas HM did not alter ASM contractility. Lactose 59-66 H19 imprinted maternally expressed transcript Homo sapiens 85-88 34159190-6 2021 In addition, both flow cytometry and 5-ethynyl-2"-deoxyuridine (EdU) assay suggested that H19 was involved in the cell cycle arrest, apoptosis, and DNA synthesis to modulate the radiation response of glioma cells and influenced their radioresistance. 5-ethynyl-2'-deoxyuridine 37-62 H19 imprinted maternally expressed transcript Homo sapiens 90-93 34159190-6 2021 In addition, both flow cytometry and 5-ethynyl-2"-deoxyuridine (EdU) assay suggested that H19 was involved in the cell cycle arrest, apoptosis, and DNA synthesis to modulate the radiation response of glioma cells and influenced their radioresistance. 5-ethynyl-2'-deoxyuridine 64-67 H19 imprinted maternally expressed transcript Homo sapiens 90-93 34401209-7 2021 The effects of lncRNA H19 on hDPSCs were achieved by repressing LATS1 through enhancer of zeste homolog 2-induced trimethylation of histone 3 at lysine 27. Lysine 145-151 H19 imprinted maternally expressed transcript Homo sapiens 22-25 34909646-8 2021 Conclusion: CM induces AHR in human ASM by eliciting an increased parasympathetic contractile response. Cm 12-14 H19 imprinted maternally expressed transcript Homo sapiens 36-39 35472411-3 2022 There is a significant body of research investigating the effects of oxidative stress/ROS on ASM behaviour, falling into the following categories; cigarette smoke and associated compounds, air pollutants, aero-allergens, asthma and COPD relevant mediators, and the anti-oxidant Nrf2/HO-1 signalling pathway. ros 86-89 H19 imprinted maternally expressed transcript Homo sapiens 93-96 35623291-0 2022 Efficacy of DMARDs and methylprednisolone treatment on the gene expression levels of HSPA5, MMD, and non-coding RNAs MALAT1, H19, miR-199a-5p, and miR-1-3p, in patients with rheumatoid arthritis. Methylprednisolone 23-41 H19 imprinted maternally expressed transcript Homo sapiens 125-128 35410483-12 2022 Adenosine supplementation activated AMPK and abolished SAHH deficiency-induced expression of H19 and Runx2 and osteoblastic differentiation of VSMCs. Adenosine 0-9 H19 imprinted maternally expressed transcript Homo sapiens 93-96 35607322-8 2022 Results: We found that TAMs-exosome treatment significantly enhanced autophagy in BC cells, and the expression of lncRNA H19 was greatly upregulated in TAMs-exosome. tams 23-27 H19 imprinted maternally expressed transcript Homo sapiens 121-124 35607322-8 2022 Results: We found that TAMs-exosome treatment significantly enhanced autophagy in BC cells, and the expression of lncRNA H19 was greatly upregulated in TAMs-exosome. tams 152-156 H19 imprinted maternally expressed transcript Homo sapiens 121-124 35607322-11 2022 At last, we found that overexpression of exosomal H19 from TAMs suppressed the interaction between ULK1 and its specific E3 ligase NEDD4L in BC cells. tams 59-63 H19 imprinted maternally expressed transcript Homo sapiens 50-53 35607322-12 2022 Conclusion: We revealed the effect of TAMs-exo-contained lncRNA H19 on regulating autophagy of bladder cancer cells, which indicated that targeting TAMs-H19 is a promising therapeutic strategy for the treatment of BC. tams 38-42 H19 imprinted maternally expressed transcript Homo sapiens 64-67 35410483-13 2022 Finally, AMPK activation by adenosine inhibited H19 expression by inducing Sirt1-mediated histone H3 hypoacetylation and DNMT3b-mediated hypermethylation of the H19 promoter in SAHH deficiency VSMCs. Adenosine 28-37 H19 imprinted maternally expressed transcript Homo sapiens 48-51 35410483-13 2022 Finally, AMPK activation by adenosine inhibited H19 expression by inducing Sirt1-mediated histone H3 hypoacetylation and DNMT3b-mediated hypermethylation of the H19 promoter in SAHH deficiency VSMCs. Adenosine 28-37 H19 imprinted maternally expressed transcript Homo sapiens 161-164 35252200-4 2022 Results: A total of 3,175 differentially expressed mRNAs (DEGs), lncRNAs (DELs), and miRNAs (DEMs) related to 5-FU resistance were identified, including significantly upregulated IL33, H19, and miR-17-5p; the downregulated AKR1B10, LINC01012, and miR-125b-5p; and chromatin modifiers such as INO80C, HDAC6, and KDM5A. Fluorouracil 110-114 H19 imprinted maternally expressed transcript Homo sapiens 185-188 35166018-0 2022 Modulation of lncRNA H19 enhances resveratrol-inhibited cancer cell proliferation and migration by regulating endoplasmic reticulum stress. Resveratrol 34-45 H19 imprinted maternally expressed transcript Homo sapiens 21-24 35220220-9 2022 There was a correlation between H19 expression and creatinine (r=0.408; p=0.003). Creatinine 51-61 H19 imprinted maternally expressed transcript Homo sapiens 32-35 35616003-14 2022 H19 was enriched in GO:0006555~methionine metabolic process, and GO:0046655~folic acid metabolic process. Methionine 31-41 H19 imprinted maternally expressed transcript Homo sapiens 0-3 35616003-14 2022 H19 was enriched in GO:0006555~methionine metabolic process, and GO:0046655~folic acid metabolic process. Folic Acid 76-86 H19 imprinted maternally expressed transcript Homo sapiens 0-3 35166018-5 2022 Results also showed that resveratrol altered the expression of several long non-coding RNAs (lncRNAs), including MEG3, PTTG3P, GAS5, BISPR, MALAT1 and H19. Resveratrol 25-36 H19 imprinted maternally expressed transcript Homo sapiens 151-154 35166018-6 2022 Knockdown of H19 in resveratrol-treated cells further enhanced the effects of resveratrol on apoptosis, ER stress and cell cycle S-phase arrest. Resveratrol 20-31 H19 imprinted maternally expressed transcript Homo sapiens 13-16 35166018-6 2022 Knockdown of H19 in resveratrol-treated cells further enhanced the effects of resveratrol on apoptosis, ER stress and cell cycle S-phase arrest. Resveratrol 78-89 H19 imprinted maternally expressed transcript Homo sapiens 13-16 35166018-7 2022 Furthermore, the migratory ability of resveratrol-treated cells was dramatically decreased after H19 knockdown. Resveratrol 38-49 H19 imprinted maternally expressed transcript Homo sapiens 97-100 35166018-8 2022 In conclusion, resveratrol inhibited cancer cell survival, while knockdown of lncRNA H19 resulted in increased sensitivity to resveratrol therapy. Resveratrol 126-137 H19 imprinted maternally expressed transcript Homo sapiens 85-88 35252200-5 2022 The construction of the ceRNA regulatory network revealed that H19, HOXA11-AS, and NEAT1 might function as ceRNAs associated with 5-FU resistance in HCT15 cells. Fluorouracil 130-134 H19 imprinted maternally expressed transcript Homo sapiens 63-66 35325980-5 2022 RESULTS: When the ASM/BMI increased by 0.1 kg/BMI, the odds for MetS and IR decreased by 36% and 29%, respectively, after adjusting for age, sex, education, economic level, smoking, alcohol consumption, physical activity, chronic diseases, and intake of fats and protein. Alcohols 182-189 H19 imprinted maternally expressed transcript Homo sapiens 18-21 35198556-4 2022 We identified that H19 was upregulated in ss-glycerophosphate (beta-GP) induced vascular smooth muscle cells (VSMCs), a cellular calcification model in vitro. ss-glycerophosphate 42-61 H19 imprinted maternally expressed transcript Homo sapiens 19-22 35125086-7 2022 Downregulation of DNMT-1, HDAC-6, miR-21, HOTAIR, and H19 with upregulation of miR-148a/miR-152 indicated that nimbolide regulates AR and IGF-1/PI3K/Akt signaling via epigenetic modifications. nimbolide 111-120 H19 imprinted maternally expressed transcript Homo sapiens 54-57 35170388-0 2022 Melatonin affects hypoxia-inducible factor 1alpha and ameliorates delayed brain injury following subarachnoid hemorrhage via H19/miR-675/HIF1A/TLR4. Melatonin 0-9 H19 imprinted maternally expressed transcript Homo sapiens 125-128 35170388-11 2022 Therefore, the treatment with MT could ameliorate post-SAH DBI.Running title: Melatonin ameliorates post-SAH DBI via H19/miR-675/HIF1A/TLR4 signaling pathways. Melatonin 78-87 H19 imprinted maternally expressed transcript Homo sapiens 117-120 35007927-0 2022 High glucose increases IGF-2/H19 expression by changing DNA methylation in HTR8/SVneo trophoblast cells. Glucose 5-12 H19 imprinted maternally expressed transcript Homo sapiens 29-32 35007927-2 2022 The aim of our study was to verify whether high glucose concentrations change the methylation levels of the insulin-like growth factor-2 (IGF-2)/H19 gene promoters to increase the expression of IGF-2, a key gene in fetal growth regulation. Glucose 48-55 H19 imprinted maternally expressed transcript Homo sapiens 145-148 35007927-6 2022 RESULTS: Among the five groups of cells, the RNA levels of IGF-2 and H19 were lowest in the 5-mM (physiological blood glucose level) group, which was statistically significant (all P < 0.05). Glucose 118-125 H19 imprinted maternally expressed transcript Homo sapiens 69-72 35007927-9 2022 DISCUSSION: High glucose concentrations may increase IGF-2/H19 expression by changing the methylation levels of the IGF-2 and H19 gene promoters. Glucose 17-24 H19 imprinted maternally expressed transcript Homo sapiens 59-62 35007927-9 2022 DISCUSSION: High glucose concentrations may increase IGF-2/H19 expression by changing the methylation levels of the IGF-2 and H19 gene promoters. Glucose 17-24 H19 imprinted maternally expressed transcript Homo sapiens 126-129 34941012-9 2022 Children with higher fecal butyric acid, acetic acid, and total SCFA levels exhibited higher TSM, ASM, TSMI, ASMI, and ASMI Z-score and lower TSM/TBF, ASM/AFM, TSMR, ASMR, and ASMR Z-score. Fatty Acids, Volatile 64-68 H19 imprinted maternally expressed transcript Homo sapiens 98-101 35087474-9 2021 AED/ASM prescription was reported to be triggered by the first clinically evident seizure with levetiracetam being the AED/ASM of choice. Levetiracetam 95-108 H19 imprinted maternally expressed transcript Homo sapiens 4-7 35087474-9 2021 AED/ASM prescription was reported to be triggered by the first clinically evident seizure with levetiracetam being the AED/ASM of choice. Levetiracetam 95-108 H19 imprinted maternally expressed transcript Homo sapiens 123-126 35121179-2 2022 Our study aimed to explore the functions of H19 in NSPCs induced by oxygen-glucose deprivation/reperfusion (OGD/R) in vitro and the underlying mechanisms. Glucose 75-82 H19 imprinted maternally expressed transcript Homo sapiens 44-47 35121179-6 2022 The results of immunofluorescence analysis revealed that H19 knockdown reduced the staining intensity of Ki-67 and DCX. KS I 105-107 H19 imprinted maternally expressed transcript Homo sapiens 57-60