<HashMap><database>JPOST Repository</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_53.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_38.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_23.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_21.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_88.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_40.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_71.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_70.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_86.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_05.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_56.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_24.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_54.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_22.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_69.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_39.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_85.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_72.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_87.raw</Raw><Raw>https://storage.jpostdb.org/JPST003922/files/I230613_55.raw</Raw></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Proteomics</omics_type><submitter>JÃ¼rgen Fritsch</submitter><species>Homo Sapiens (human)</species><full_dataset_link>https://repository.jpostdb.org/entry/JPST003922</full_dataset_link><submitter_affiliation>Insitute of Immunology, University Medical Center Mainz</submitter_affiliation><sample_protocol></sample_protocol><repository>jPOST</repository><data_protocol></data_protocol></additional><is_claimable>false</is_claimable><name>Loss of ADAM15 prevents necroptosis induction by partial RIPK1 degradation and altered organelle organization.</name><description>Death receptor-mediated signaling pathways must be tightly regulated to ensure tissue homeostasis. In a previous study, ADAM15 was identified as a possible TNF-regulated protease. We here unveil ADAM15 as a regulator of TNF-mediated necroptosis, while apoptosis and survival pathways remain unaffected. ADAM15 knockout results in the modulation of death-associated proteins and protein networks. Using a bottom-up proteomics screen to compare human U937 wild-type and ADAM15 knockdown cells enabled us to identify proteins and networks affected by ADAM15 loss, and which may be involved in necroptosis regulation.</description><dates><publication>Sat Jul 11 00:00:00 GMT+01:00 2026</publication></dates><accession>PXD066056</accession><cross_references><TAXONOMY>9606</TAXONOMY></cross_references></HashMap>