{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Konig SM"],"funding":["ISCRA CINECA","Carlsbergfondet","Danmarks Grundforskningsfond","LEO Foundation","Novo Nordisk Foundation Center for Protein Research","Partnership for Advanced Computing in Europe AISBL","LEO Fondet"],"pagination":["e1007485"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6927658"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(12)"],"pubmed_abstract":["Apoptosis is an essential defensive mechanism against tumorigenesis. Proteins of the B-cell lymphoma-2 (Bcl-2) family regulate programmed cell death by the mitochondrial apoptosis pathway. In response to intracellular stress, the apoptotic balance is governed by interactions of three distinct subgroups of proteins; the activator/sensitizer BH3 (Bcl-2 homology 3)-only proteins, the pro-survival, and the pro-apoptotic executioner proteins. Changes in expression levels, stability, and functional impairment of pro-survival proteins can lead to an imbalance in tissue homeostasis. Their overexpression or hyperactivation can result in oncogenic effects. Pro-survival Bcl-2 family members carry out their function by binding the BH3 short linear motif of pro-apoptotic proteins in a modular way, crea"],"journal":["PLoS computational biology"],"pubmed_title":["Alterations of the interactome of Bcl-2 proteins in breast cancer at the transcriptional, mutational and structural level."],"pmcid":["PMC6927658"],"funding_grant_id":["DNRF125","PI Søren Brunak","CF18-0314","P10C8YXRK","HP10CBLBWO","DECI-15th","DECI-14th","LF17006"],"pubmed_authors":["Lambrughi M","Konig SM","Rissler V","Terkelsen T","Papaleo E"],"additional_accession":[]},"is_claimable":false,"name":"Alterations of the interactome of Bcl-2 proteins in breast cancer at the transcriptional, mutational and structural level.","description":"Apoptosis is an essential defensive mechanism against tumorigenesis. Proteins of the B-cell lymphoma-2 (Bcl-2) family regulate programmed cell death by the mitochondrial apoptosis pathway. In response to intracellular stress, the apoptotic balance is governed by interactions of three distinct subgroups of proteins; the activator/sensitizer BH3 (Bcl-2 homology 3)-only proteins, the pro-survival, and the pro-apoptotic executioner proteins. Changes in expression levels, stability, and functional impairment of pro-survival proteins can lead to an imbalance in tissue homeostasis. Their overexpression or hyperactivation can result in oncogenic effects. Pro-survival Bcl-2 family members carry out their function by binding the BH3 short linear motif of pro-apoptotic proteins in a modular way, crea","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2026-05-04T09:23:03.153Z","creation":"2020-05-22T07:18:01Z"},"accession":"S-EPMC6927658","cross_references":{"pubmed":["31825969"],"doi":["10.1371/journal.pcbi.1007485"]}}