Differential cell cycle perturbation by transmethylation inhibitors
Cell cycle distribution of HL-60 cells was studied by flow cytometry after incubation with the transmethylation inhibitors 3-deaza-(±)-aristeromycin (c 3Ari) and 3-deazaadenosine (c 3Ado). Cells were incubated with the drugs (25 μM) for two cell doublings in control cells (36 hr). The presence of c...
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| Veröffentlicht in: | Biochemical pharmacology 1990, Vol.39 (1), p.203-206 |
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| creator | Prytz, Per S. Aarbakke, Jarle |
| description | Cell cycle distribution of HL-60 cells was studied by flow cytometry after incubation with the transmethylation inhibitors 3-deaza-(±)-aristeromycin (c
3Ari) and 3-deazaadenosine (c
3Ado). Cells were incubated with the drugs (25 μM) for two cell doublings in control cells (36 hr). The presence of c
3Ari caused a dose-dependent, reversible G
2+M arrest, whereas c
3Ado-treated cells accumulated in G
0/G
1,. The G
2+M arrest was also found in NIH/3T3 cells incubated for 36 hr with 25μM c
3Ari, but not in U937 and K562 cells. Possible mechanisms for the described effects of c
3Ari are discussed from the perspective that inhibition of
S-adenosyl homocysteine hydrolase, and subsequent inhibition of transmethylation reactions, at present is the only known site of action of c
3Ari. |
| doi_str_mv | 10.1016/0006-2952(90)90666-9 |
| format | Article |
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3Ari) and 3-deazaadenosine (c
3Ado). Cells were incubated with the drugs (25 μM) for two cell doublings in control cells (36 hr). The presence of c
3Ari caused a dose-dependent, reversible G
2+M arrest, whereas c
3Ado-treated cells accumulated in G
0/G
1,. The G
2+M arrest was also found in NIH/3T3 cells incubated for 36 hr with 25μM c
3Ari, but not in U937 and K562 cells. Possible mechanisms for the described effects of c
3Ari are discussed from the perspective that inhibition of
S-adenosyl homocysteine hydrolase, and subsequent inhibition of transmethylation reactions, at present is the only known site of action of c
3Ari.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/0006-2952(90)90666-9</identifier><identifier>PMID: 2297355</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenosine - analogs & derivatives ; Adenosine - pharmacology ; Adenosylhomocysteinase ; Aminoglycosides ; Anti-Bacterial Agents - pharmacology ; Biological and medical sciences ; Cell Cycle - drug effects ; Cell cycle, cell proliferation ; Cell physiology ; Enzyme Inhibitors ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; Humans ; Hydrolases - antagonists & inhibitors ; Interphase - drug effects ; Kinetics ; Leukemia, Promyelocytic, Acute ; Methylation ; Mitosis - drug effects ; Molecular and cellular biology ; Tubercidin - pharmacology ; Tumor Cells, Cultured</subject><ispartof>Biochemical pharmacology, 1990, Vol.39 (1), p.203-206</ispartof><rights>1989</rights><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-3cdf8012219d7f5966f405a5ea00c99ebae468cd495552114dbda2dc923567783</citedby><cites>FETCH-LOGICAL-c417t-3cdf8012219d7f5966f405a5ea00c99ebae468cd495552114dbda2dc923567783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0006-2952(90)90666-9$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6718082$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2297355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prytz, Per S.</creatorcontrib><creatorcontrib>Aarbakke, Jarle</creatorcontrib><title>Differential cell cycle perturbation by transmethylation inhibitors</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Cell cycle distribution of HL-60 cells was studied by flow cytometry after incubation with the transmethylation inhibitors 3-deaza-(±)-aristeromycin (c
3Ari) and 3-deazaadenosine (c
3Ado). Cells were incubated with the drugs (25 μM) for two cell doublings in control cells (36 hr). The presence of c
3Ari caused a dose-dependent, reversible G
2+M arrest, whereas c
3Ado-treated cells accumulated in G
0/G
1,. The G
2+M arrest was also found in NIH/3T3 cells incubated for 36 hr with 25μM c
3Ari, but not in U937 and K562 cells. Possible mechanisms for the described effects of c
3Ari are discussed from the perspective that inhibition of
S-adenosyl homocysteine hydrolase, and subsequent inhibition of transmethylation reactions, at present is the only known site of action of c
3Ari.</description><subject>Adenosine - analogs & derivatives</subject><subject>Adenosine - pharmacology</subject><subject>Adenosylhomocysteinase</subject><subject>Aminoglycosides</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Cycle - drug effects</subject><subject>Cell cycle, cell proliferation</subject><subject>Cell physiology</subject><subject>Enzyme Inhibitors</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Hydrolases - antagonists & inhibitors</subject><subject>Interphase - drug effects</subject><subject>Kinetics</subject><subject>Leukemia, Promyelocytic, Acute</subject><subject>Methylation</subject><subject>Mitosis - drug effects</subject><subject>Molecular and cellular biology</subject><subject>Tubercidin - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LxDAQhoMo67r6DxT2IKKHapI2SXMRZP2EBS96DmkyxUi3XZNU6L-3tWWPesmQmWeGlwehU4KvCSb8BmPMEyoZvZT4SmLOeSL30JzkIu3bPN9H8x1yiI5C-By-OSczNKNUipSxOVrdu7IED3V0uloaqPqnMxUst-Bj6wsdXVMvi24Zva7DBuJHV409V3-4wsXGh2N0UOoqwMlUF-j98eFt9ZysX59eVnfrxGRExCQ1tswxoZRIK0omOS8zzDQDjbGREgoNGc-NzSRjjBKS2cJqao2kKeNC5OkCXYx3t775aiFEtXFhiKxraNqghGSS0JT-CxImhEgp68FsBI1vQvBQqq13G-07RbAaJKtBmRoMKonVr2Ql-7Wz6X5bbMDuliar_fx8mutgdFX26owLO4wLkuN8iHk7YtBL-3bgVTAOagPWeTBR2cb9neMH6keX8Q</recordid><startdate>1990</startdate><enddate>1990</enddate><creator>Prytz, Per S.</creator><creator>Aarbakke, Jarle</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>1990</creationdate><title>Differential cell cycle perturbation by transmethylation inhibitors</title><author>Prytz, Per S. ; Aarbakke, Jarle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-3cdf8012219d7f5966f405a5ea00c99ebae468cd495552114dbda2dc923567783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Adenosine - analogs & derivatives</topic><topic>Adenosine - pharmacology</topic><topic>Adenosylhomocysteinase</topic><topic>Aminoglycosides</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Cycle - drug effects</topic><topic>Cell cycle, cell proliferation</topic><topic>Cell physiology</topic><topic>Enzyme Inhibitors</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Hydrolases - antagonists & inhibitors</topic><topic>Interphase - drug effects</topic><topic>Kinetics</topic><topic>Leukemia, Promyelocytic, Acute</topic><topic>Methylation</topic><topic>Mitosis - drug effects</topic><topic>Molecular and cellular biology</topic><topic>Tubercidin - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prytz, Per S.</creatorcontrib><creatorcontrib>Aarbakke, Jarle</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prytz, Per S.</au><au>Aarbakke, Jarle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential cell cycle perturbation by transmethylation inhibitors</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>1990</date><risdate>1990</risdate><volume>39</volume><issue>1</issue><spage>203</spage><epage>206</epage><pages>203-206</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Cell cycle distribution of HL-60 cells was studied by flow cytometry after incubation with the transmethylation inhibitors 3-deaza-(±)-aristeromycin (c
3Ari) and 3-deazaadenosine (c
3Ado). Cells were incubated with the drugs (25 μM) for two cell doublings in control cells (36 hr). The presence of c
3Ari caused a dose-dependent, reversible G
2+M arrest, whereas c
3Ado-treated cells accumulated in G
0/G
1,. The G
2+M arrest was also found in NIH/3T3 cells incubated for 36 hr with 25μM c
3Ari, but not in U937 and K562 cells. Possible mechanisms for the described effects of c
3Ari are discussed from the perspective that inhibition of
S-adenosyl homocysteine hydrolase, and subsequent inhibition of transmethylation reactions, at present is the only known site of action of c
3Ari.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>2297355</pmid><doi>10.1016/0006-2952(90)90666-9</doi><tpages>4</tpages></addata></record> |
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| ispartof | Biochemical pharmacology, 1990, Vol.39 (1), p.203-206 |
| issn | 0006-2952 1873-2968 |
| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Adenosine - analogs & derivatives Adenosine - pharmacology Adenosylhomocysteinase Aminoglycosides Anti-Bacterial Agents - pharmacology Biological and medical sciences Cell Cycle - drug effects Cell cycle, cell proliferation Cell physiology Enzyme Inhibitors Flow Cytometry Fundamental and applied biological sciences. Psychology Humans Hydrolases - antagonists & inhibitors Interphase - drug effects Kinetics Leukemia, Promyelocytic, Acute Methylation Mitosis - drug effects Molecular and cellular biology Tubercidin - pharmacology Tumor Cells, Cultured |
| title | Differential cell cycle perturbation by transmethylation inhibitors |
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