Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.
Identifieur interne : 000368 ( Main/Corpus ); précédent : 000367; suivant : 000369Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.
Auteurs : Xue Gao ; Yuming Zhou ; Hongliu Sun ; Desheng Liu ; Jing Zhang ; Junru Zhang ; Weizhong Liu ; Xiaohong PanSource :
- Toxicology and applied pharmacology [ 1096-0333 ] ; 2019.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (metabolism), Animals (MeSH), Antineoplastic Agents (pharmacology), Antineoplastic Agents (toxicity), Apoptosis (drug effects), Apoptosis Regulatory Proteins (metabolism), Autophagy (drug effects), Autophagy-Related Proteins (metabolism), Cell Cycle Checkpoints (drug effects), Cell Proliferation (MeSH), Chromatography, High Pressure Liquid (MeSH), HL-60 Cells (MeSH), Humans (MeSH), K562 Cells (MeSH), Leukemia (drug therapy), Leukemia (metabolism), Leukemia (pathology), Mice (MeSH), Proteomics (methods), Pyrans (pharmacology), Pyrans (toxicity), Signal Transduction (drug effects), Spiro Compounds (pharmacology), Spiro Compounds (toxicity), THP-1 Cells (MeSH), TOR Serine-Threonine Kinases (metabolism), Tandem Mass Spectrometry (MeSH).
- MESH :
- chemical , metabolism : AMP-Activated Protein Kinases, Apoptosis Regulatory Proteins, Autophagy-Related Proteins, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Antineoplastic Agents, Pyrans, Spiro Compounds.
- chemical , toxicity : Antineoplastic Agents, Pyrans, Spiro Compounds.
- drug effects : Apoptosis, Autophagy, Cell Cycle Checkpoints, Signal Transduction.
- drug therapy : Leukemia.
- metabolism : Leukemia.
- methods : Proteomics.
- pathology : Leukemia.
- Animals, Cell Proliferation, Chromatography, High Pressure Liquid, HL-60 Cells, Humans, K562 Cells, Mice, THP-1 Cells, Tandem Mass Spectrometry.
Abstract
Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.
DOI: 10.1016/j.taap.2018.12.007
PubMed: 30660475
Links to Exploration step
pubmed:30660475Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.</title><author><name sortKey="Gao, Xue" sort="Gao, Xue" uniqKey="Gao X" first="Xue" last="Gao">Xue Gao</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Yuming" sort="Zhou, Yuming" uniqKey="Zhou Y" first="Yuming" last="Zhou">Yuming Zhou</name><affiliation><nlm:affiliation>Affiliated Hospital of Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Sun, Hongliu" sort="Sun, Hongliu" uniqKey="Sun H" first="Hongliu" last="Sun">Hongliu Sun</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Desheng" sort="Liu, Desheng" uniqKey="Liu D" first="Desheng" last="Liu">Desheng Liu</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Junru" sort="Zhang, Junru" uniqKey="Zhang J" first="Junru" last="Zhang">Junru Zhang</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Weizhong" sort="Liu, Weizhong" uniqKey="Liu W" first="Weizhong" last="Liu">Weizhong Liu</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: lwz1963@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Pan, Xiaohong" sort="Pan, Xiaohong" uniqKey="Pan X" first="Xiaohong" last="Pan">Xiaohong Pan</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: panxiaohong@bzmc.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:30660475</idno><idno type="pmid">30660475</idno><idno type="doi">10.1016/j.taap.2018.12.007</idno><idno type="wicri:Area/Main/Corpus">000368</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000368</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.</title><author><name sortKey="Gao, Xue" sort="Gao, Xue" uniqKey="Gao X" first="Xue" last="Gao">Xue Gao</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhou, Yuming" sort="Zhou, Yuming" uniqKey="Zhou Y" first="Yuming" last="Zhou">Yuming Zhou</name><affiliation><nlm:affiliation>Affiliated Hospital of Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Sun, Hongliu" sort="Sun, Hongliu" uniqKey="Sun H" first="Hongliu" last="Sun">Hongliu Sun</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Desheng" sort="Liu, Desheng" uniqKey="Liu D" first="Desheng" last="Liu">Desheng Liu</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Junru" sort="Zhang, Junru" uniqKey="Zhang J" first="Junru" last="Zhang">Junru Zhang</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Weizhong" sort="Liu, Weizhong" uniqKey="Liu W" first="Weizhong" last="Liu">Weizhong Liu</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: lwz1963@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Pan, Xiaohong" sort="Pan, Xiaohong" uniqKey="Pan X" first="Xiaohong" last="Pan">Xiaohong Pan</name><affiliation><nlm:affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: panxiaohong@bzmc.edu.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Toxicology and applied pharmacology</title><idno type="eISSN">1096-0333</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (metabolism)</term><term>Animals (MeSH)</term><term>Antineoplastic Agents (pharmacology)</term><term>Antineoplastic Agents (toxicity)</term><term>Apoptosis (drug effects)</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Autophagy (drug effects)</term><term>Autophagy-Related Proteins (metabolism)</term><term>Cell Cycle Checkpoints (drug effects)</term><term>Cell Proliferation (MeSH)</term><term>Chromatography, High Pressure Liquid (MeSH)</term><term>HL-60 Cells (MeSH)</term><term>Humans (MeSH)</term><term>K562 Cells (MeSH)</term><term>Leukemia (drug therapy)</term><term>Leukemia (metabolism)</term><term>Leukemia (pathology)</term><term>Mice (MeSH)</term><term>Proteomics (methods)</term><term>Pyrans (pharmacology)</term><term>Pyrans (toxicity)</term><term>Signal Transduction (drug effects)</term><term>Spiro Compounds (pharmacology)</term><term>Spiro Compounds (toxicity)</term><term>THP-1 Cells (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Tandem Mass Spectrometry (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term><term>Apoptosis Regulatory Proteins</term><term>Autophagy-Related Proteins</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Pyrans</term><term>Spiro Compounds</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Antineoplastic Agents</term><term>Pyrans</term><term>Spiro Compounds</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Cycle Checkpoints</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Leukemia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Leukemia</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Proteomics</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Leukemia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Proliferation</term><term>Chromatography, High Pressure Liquid</term><term>HL-60 Cells</term><term>Humans</term><term>K562 Cells</term><term>Mice</term><term>THP-1 Cells</term><term>Tandem Mass Spectrometry</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30660475</PMID><DateCompleted><Year>2019</Year><Month>10</Month><Day>29</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0333</ISSN><JournalIssue CitedMedium="Internet"><Volume>366</Volume><PubDate><Year>2019</Year><Month>03</Month><Day>01</Day></PubDate></JournalIssue><Title>Toxicology and applied pharmacology</Title><ISOAbbreviation>Toxicol Appl Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.</ArticleTitle><Pagination><MedlinePgn>1-9</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0041-008X(18)30543-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.taap.2018.12.007</ELocationID><Abstract><AbstractText>Peniciketal A (Pe-A), a spiroketal compound, is isolated from the saline soil-derived fungus Penicillium raistrickii. However, the underlying molecular mechanistic basis for the effects of Pe-A on leukemia is poorly understood. Here, we investigated that Pe-A reduced cell proliferation in three leukemia cell lines (THP-1, K562 and HL60). Importantly, Pe-A showed little cytotoxicity in primary mouse embryonic fibroblast (MEF) cells in a long-duration treatment. For the mechanistic research, we identified 3449 differentially expressed Pe-A-induced proteins through liquid chromatography-tandem mass spectrometry (LC-MS/MS) with TMT label in THP-1 cells. Results showed that many identified proteins were involved in apoptosis and/or autophagy. Then, we confirmed that Pe-A induced not only apoptosis via the mitochondrial pathway but also cytoprotective autophagy by activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway indeed. In addition, Pe-A also arrested the cell cycle at the G0-G1 phase by regulating the expressions of checkpoint protein. Collectively, these results provide new insights into the mechanisms that Pe-A may target autophagy-related or apoptosis-related pathways to suppress the development of human leukemia.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Xue</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Yuming</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Affiliated Hospital of Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Hongliu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Desheng</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Junru</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Weizhong</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: lwz1963@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Xiaohong</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China. Electronic address: panxiaohong@bzmc.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>01</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Toxicol Appl Pharmacol</MedlineTA><NlmUniqueID>0416575</NlmUniqueID><ISSNLinking>0041-008X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051017">Apoptosis Regulatory Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071183">Autophagy-Related Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011714">Pyrans</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013141">Spiro Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C587991">peniciketal A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber><NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051017" MajorTopicYN="N">Apoptosis Regulatory Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071183" MajorTopicYN="N">Autophagy-Related Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059447" MajorTopicYN="N">Cell Cycle Checkpoints</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="Y">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018922" MajorTopicYN="N">HL-60 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020014" MajorTopicYN="N">K562 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007938" MajorTopicYN="N">Leukemia</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040901" MajorTopicYN="N">Proteomics</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011714" MajorTopicYN="N">Pyrans</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013141" MajorTopicYN="N">Spiro Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000074084" MajorTopicYN="N">THP-1 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053719" MajorTopicYN="N">Tandem Mass Spectrometry</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Apoptosis</Keyword><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Leukemia</Keyword><Keyword MajorTopicYN="Y">Peniciketal A</Keyword><Keyword MajorTopicYN="Y">Proteomics</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>10</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>12</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>12</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>10</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30660475</ArticleId><ArticleId IdType="pii">S0041-008X(18)30543-X</ArticleId><ArticleId IdType="doi">10.1016/j.taap.2018.12.007</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000368 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000368 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:30660475
|texte= Effects of a spiroketal compound Peniciketal A and its molecular mechanisms on growth inhibition in human leukemia.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:30660475" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |