Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.
Identifieur interne : 000158 ( Main/Exploration ); précédent : 000157; suivant : 000159Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.
Auteurs : Jean Jung [Corée du Sud] ; Eunbyul Yeom [Corée du Sud] ; Kwang-Wook Choi [Corée du Sud]Source :
- Cell death & disease [ 2041-4889 ] ; 2020.
Abstract
Ciao1 is a component of the cytosolic iron-sulfur cluster assembly (CIA) complex along with MMS19 and MIP18. Xeroderma pigmentosum group D (XPD), a DNA helicase involved in regulation of cell cycle and transcription, is a CIA target for iron-sulfur (Fe/S) modification. In vivo function of Ciao1 and Xpd in developing animals has been rarely studied. Here, we reveal that Ciao1 interacts with Crumbs (Crb), Galla, and Xpd to regulate organ growth in Drosophila. Abnormal growth of eye by overexpressing Crb intracellular domain (Crbintra) is suppressed by reducing the Ciao1 level. Loss of Ciao1 or Xpd causes similar impairment in organ growth. RNAi knockdown of both Ciao1 and Xpd show similar phenotypes as Ciao1 or Xpd RNAi alone, suggesting their function in a pathway. Growth defects caused by Ciao1 RNAi are suppressed by overexpression of Xpd. Ciao1 physically interacts with Crbintra, Galla, and Xpd, supporting their genetic interactions. Remarkably, Xpd RNAi defects can also be suppressed by Ciao1 overexpression, implying a mutual regulation between the two genes. Ciao1 mutant clones in imaginal discs show decreased levels of Cyclin E (CycE) and death-associated inhibitor of apoptosis 1 (Diap1). Xpd mutant clones share the similar reduction of CycE and Diap1. Consequently, knockdown of Ciao1 and Xpd by RNAi show increased apoptotic cell death. Further, CycE overexpression is sufficient to restore the growth defects from Ciao1 RNAi or Xpd RNAi. Interestingly, Diap1 overexpression in Ciao1 mutant clones induces CycE expression, suggesting that reduced CycE in Ciao1 mutant cells is secondary to loss of Diap1. Taken together, this study reveals new roles of Ciao1 and Xpd in cell survival and growth through regulating Diap1 level during organ development.
DOI: 10.1038/s41419-020-2564-3
PubMed: 32404863
PubMed Central: PMC7220951
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.</title><author><name sortKey="Jung, Jean" sort="Jung, Jean" uniqKey="Jung J" first="Jean" last="Jung">Jean Jung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author><author><name sortKey="Yeom, Eunbyul" sort="Yeom, Eunbyul" uniqKey="Yeom E" first="Eunbyul" last="Yeom">Eunbyul Yeom</name><affiliation wicri:level="1"><nlm:affiliation>Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author><author><name sortKey="Choi, Kwang Wook" sort="Choi, Kwang Wook" uniqKey="Choi K" first="Kwang-Wook" last="Choi">Kwang-Wook Choi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea. kchoi100@kaist.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32404863</idno><idno type="pmid">32404863</idno><idno type="doi">10.1038/s41419-020-2564-3</idno><idno type="pmc">PMC7220951</idno><idno type="wicri:Area/Main/Corpus">000093</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000093</idno><idno type="wicri:Area/Main/Curation">000093</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000093</idno><idno type="wicri:Area/Main/Exploration">000093</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.</title><author><name sortKey="Jung, Jean" sort="Jung, Jean" uniqKey="Jung J" first="Jean" last="Jung">Jean Jung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author><author><name sortKey="Yeom, Eunbyul" sort="Yeom, Eunbyul" uniqKey="Yeom E" first="Eunbyul" last="Yeom">Eunbyul Yeom</name><affiliation wicri:level="1"><nlm:affiliation>Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author><author><name sortKey="Choi, Kwang Wook" sort="Choi, Kwang Wook" uniqKey="Choi K" first="Kwang-Wook" last="Choi">Kwang-Wook Choi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea. kchoi100@kaist.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141</wicri:regionArea><wicri:noRegion>34141</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell death & disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ciao1 is a component of the cytosolic iron-sulfur cluster assembly (CIA) complex along with MMS19 and MIP18. Xeroderma pigmentosum group D (XPD), a DNA helicase involved in regulation of cell cycle and transcription, is a CIA target for iron-sulfur (Fe/S) modification. In vivo function of Ciao1 and Xpd in developing animals has been rarely studied. Here, we reveal that Ciao1 interacts with Crumbs (Crb), Galla, and Xpd to regulate organ growth in Drosophila. Abnormal growth of eye by overexpressing Crb intracellular domain (Crb<sup>intra</sup>) is suppressed by reducing the Ciao1 level. Loss of Ciao1 or Xpd causes similar impairment in organ growth. RNAi knockdown of both Ciao1 and Xpd show similar phenotypes as Ciao1 or Xpd RNAi alone, suggesting their function in a pathway. Growth defects caused by Ciao1 RNAi are suppressed by overexpression of Xpd. Ciao1 physically interacts with Crb<sup>intra</sup>, Galla, and Xpd, supporting their genetic interactions. Remarkably, Xpd RNAi defects can also be suppressed by Ciao1 overexpression, implying a mutual regulation between the two genes. Ciao1 mutant clones in imaginal discs show decreased levels of Cyclin E (CycE) and death-associated inhibitor of apoptosis 1 (Diap1). Xpd mutant clones share the similar reduction of CycE and Diap1. Consequently, knockdown of Ciao1 and Xpd by RNAi show increased apoptotic cell death. Further, CycE overexpression is sufficient to restore the growth defects from Ciao1 RNAi or Xpd RNAi. Interestingly, Diap1 overexpression in Ciao1 mutant clones induces CycE expression, suggesting that reduced CycE in Ciao1 mutant cells is secondary to loss of Diap1. Taken together, this study reveals new roles of Ciao1 and Xpd in cell survival and growth through regulating Diap1 level during organ development.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">32404863</PMID><DateRevised><Year>2020</Year><Month>05</Month><Day>16</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-4889</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>5</Issue><PubDate><Year>2020</Year><Month>May</Month><Day>13</Day></PubDate></JournalIssue><Title>Cell death & disease</Title><ISOAbbreviation>Cell Death Dis</ISOAbbreviation></Journal><ArticleTitle>Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.</ArticleTitle><Pagination><MedlinePgn>365</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41419-020-2564-3</ELocationID><Abstract><AbstractText>Ciao1 is a component of the cytosolic iron-sulfur cluster assembly (CIA) complex along with MMS19 and MIP18. Xeroderma pigmentosum group D (XPD), a DNA helicase involved in regulation of cell cycle and transcription, is a CIA target for iron-sulfur (Fe/S) modification. In vivo function of Ciao1 and Xpd in developing animals has been rarely studied. Here, we reveal that Ciao1 interacts with Crumbs (Crb), Galla, and Xpd to regulate organ growth in Drosophila. Abnormal growth of eye by overexpressing Crb intracellular domain (Crb<sup>intra</sup>) is suppressed by reducing the Ciao1 level. Loss of Ciao1 or Xpd causes similar impairment in organ growth. RNAi knockdown of both Ciao1 and Xpd show similar phenotypes as Ciao1 or Xpd RNAi alone, suggesting their function in a pathway. Growth defects caused by Ciao1 RNAi are suppressed by overexpression of Xpd. Ciao1 physically interacts with Crb<sup>intra</sup>, Galla, and Xpd, supporting their genetic interactions. Remarkably, Xpd RNAi defects can also be suppressed by Ciao1 overexpression, implying a mutual regulation between the two genes. Ciao1 mutant clones in imaginal discs show decreased levels of Cyclin E (CycE) and death-associated inhibitor of apoptosis 1 (Diap1). Xpd mutant clones share the similar reduction of CycE and Diap1. Consequently, knockdown of Ciao1 and Xpd by RNAi show increased apoptotic cell death. Further, CycE overexpression is sufficient to restore the growth defects from Ciao1 RNAi or Xpd RNAi. Interestingly, Diap1 overexpression in Ciao1 mutant clones induces CycE expression, suggesting that reduced CycE in Ciao1 mutant cells is secondary to loss of Diap1. Taken together, this study reveals new roles of Ciao1 and Xpd in cell survival and growth through regulating Diap1 level during organ development.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Jean</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yeom</LastName><ForeName>Eunbyul</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Kwang-Wook</ForeName><Initials>KW</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea. kchoi100@kaist.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2014K1A1A2042982</GrantID><Agency>National Research Foundation of Korea (NRF)</Agency><Country></Country></Grant><Grant><GrantID>2017R1A2B3007516</GrantID><Agency>National Research Foundation of Korea (NRF)</Agency><Country></Country></Grant><Grant><GrantID>2014K1A1A2042982</GrantID><Agency>National Research Foundation of Korea (NRF)</Agency><Country></Country></Grant><Grant><GrantID>2017R1A2B3007516</GrantID><Agency>National Research Foundation of Korea (NRF)</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Death Dis</MedlineTA><NlmUniqueID>101524092</NlmUniqueID></MedlineJournalInfo><CitationSubset>IM</CitationSubset></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>04</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>04</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32404863</ArticleId><ArticleId IdType="doi">10.1038/s41419-020-2564-3</ArticleId><ArticleId IdType="pii">10.1038/s41419-020-2564-3</ArticleId><ArticleId IdType="pmc">PMC7220951</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Proc Natl Acad Sci U S A. 2010 Sep 7;107(36):15810-5</Citation><ArticleIdList><ArticleId IdType="pubmed">20798049</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2010 Jun 8;107(23):10532-7</Citation><ArticleIdList><ArticleId IdType="pubmed">20498073</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochimie. 2003 Nov;85(11):1101-11</Citation><ArticleIdList><ArticleId IdType="pubmed">14726016</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2005 Dec;25(24):10833-41</Citation><ArticleIdList><ArticleId IdType="pubmed">16314508</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Cell Biol. 2002 Jun;4(6):432-8</Citation><ArticleIdList><ArticleId IdType="pubmed">12021769</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2015 May 29;290(22):14218-25</Citation><ArticleIdList><ArticleId IdType="pubmed">25897079</ArticleId></ArticleIdList></Reference><Reference><Citation>Dev Biol. 1975 Feb;42(2):211-21</Citation><ArticleIdList><ArticleId IdType="pubmed">1116643</ArticleId></ArticleIdList></Reference><Reference><Citation>Development. 1995 Oct;121(10):3371-9</Citation><ArticleIdList><ArticleId IdType="pubmed">7588070</ArticleId></ArticleIdList></Reference><Reference><Citation>Structure. 2007 Oct;15(10):1246-57</Citation><ArticleIdList><ArticleId IdType="pubmed">17937914</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochemistry. 2010 Jun 22;49(24):4945-56</Citation><ArticleIdList><ArticleId IdType="pubmed">20481466</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Biol. 2002 Sep 2;158(5):941-51</Citation><ArticleIdList><ArticleId IdType="pubmed">12213838</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 1995 Dec 29;83(7):1253-62</Citation><ArticleIdList><ArticleId IdType="pubmed">8548811</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2002 Mar 14;416(6877):143-9</Citation><ArticleIdList><ArticleId IdType="pubmed">11850625</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell. 2006 Sep 15;23(6):801-8</Citation><ArticleIdList><ArticleId IdType="pubmed">16973432</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncogene. 2015 May 21;34(21):2777-89</Citation><ArticleIdList><ArticleId IdType="pubmed">25065591</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell. 2010 Aug 27;39(4):632-40</Citation><ArticleIdList><ArticleId IdType="pubmed">20797633</ArticleId></ArticleIdList></Reference><Reference><Citation>Genetics. 1999 Aug;152(4):1631-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10430588</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2002 Mar 14;416(6877):178-83</Citation><ArticleIdList><ArticleId IdType="pubmed">11850624</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2011 Oct 28;147(3):690-703</Citation><ArticleIdList><ArticleId IdType="pubmed">22036573</ArticleId></ArticleIdList></Reference><Reference><Citation>Development. 1993 Apr;117(4):1223-37</Citation><ArticleIdList><ArticleId IdType="pubmed">8404527</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2008 May 30;133(5):801-12</Citation><ArticleIdList><ArticleId IdType="pubmed">18510925</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Protoc. 2006;1(6):2583-9</Citation><ArticleIdList><ArticleId IdType="pubmed">17406512</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Biol. 2010 Apr 13;20(7):582-90</Citation><ArticleIdList><ArticleId IdType="pubmed">20362445</ArticleId></ArticleIdList></Reference><Reference><Citation>Anal Biochem. 1993 Apr;210(1):179-87</Citation><ArticleIdList><ArticleId IdType="pubmed">8489015</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1997 Aug 1;277(5326):653-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9235882</ArticleId></ArticleIdList></Reference><Reference><Citation>Development. 1993 Jun;118(2):401-15</Citation><ArticleIdList><ArticleId IdType="pubmed">8223268</ArticleId></ArticleIdList></Reference><Reference><Citation>Development. 2018 Jan 25;145(2):</Citation><ArticleIdList><ArticleId IdType="pubmed">29361561</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Cell Biol. 2002 Jun;4(6):445-50</Citation><ArticleIdList><ArticleId IdType="pubmed">12021771</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12712-7</Citation><ArticleIdList><ArticleId IdType="pubmed">14569003</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuroscience. 2007 Apr 14;145(4):1388-96</Citation><ArticleIdList><ArticleId IdType="pubmed">17276014</ArticleId></ArticleIdList></Reference><Reference><Citation>Dev Biol. 1976 Oct 15;53(2):217-40</Citation><ArticleIdList><ArticleId IdType="pubmed">825400</ArticleId></ArticleIdList></Reference><Reference><Citation>Development. 1991 Nov;113(3):841-50</Citation><ArticleIdList><ArticleId IdType="pubmed">1726564</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2001 Jan 1;15(1):15-23</Citation><ArticleIdList><ArticleId IdType="pubmed">11156600</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1998 May 1;273(18):10880-7</Citation><ArticleIdList><ArticleId IdType="pubmed">9556563</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Genet. 2008 Nov;4(11):e1000253</Citation><ArticleIdList><ArticleId IdType="pubmed">19008953</ArticleId></ArticleIdList></Reference><Reference><Citation>DNA Repair (Amst). 2016 Aug;44:136-142</Citation><ArticleIdList><ArticleId IdType="pubmed">27262611</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Jung, Jean" sort="Jung, Jean" uniqKey="Jung J" first="Jean" last="Jung">Jean Jung</name></noRegion><name sortKey="Choi, Kwang Wook" sort="Choi, Kwang Wook" uniqKey="Choi K" first="Kwang-Wook" last="Choi">Kwang-Wook Choi</name><name sortKey="Yeom, Eunbyul" sort="Yeom, Eunbyul" uniqKey="Yeom E" first="Eunbyul" last="Yeom">Eunbyul Yeom</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/IronSulferCluV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000158 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000158 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= IronSulferCluV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:32404863
|texte= Ciao1 interacts with Crumbs and Xpd to regulate organ growth in Drosophila.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:32404863" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a IronSulferCluV1
| This area was generated with Dilib version V0.6.38. |  |