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Biomolecules publishes reviews, regular research papers and short communications. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. 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Recently, FKBP51 has been implicated in several cellular pathways and numerous interacting protein partners have been reported. However, no consensus on the underlying molecular mechanisms has yet emerged. Here, we review the protein interaction partners reported for FKBP51, the proposed pathways involved, their relevance to FKBP51’s physiological function(s), the interplay with other FKBPs, and implications for the development of FKBP51-directed drugs.\u003C\u002Fjats:p>",{"EN":119},"The Many Faces of FKBP51",{"VOID":121},"30669684",{"VOID":123},"10.3390\u002Fbiom9010035","PUBLICATION","VERIFIED","Auto 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2003, Structure of the large FK506-binding protein FKBP51, an Hsp90-binding protein and a component of steroid receptor complexes, Proc. Natl. Acad. Sci. USA, 100, 868, 10.1073\u002Fpnas.0231020100",{"doi":265},"10.1073\u002Fpnas.0231020100",{"id":21,"text":267,"url":21,"identifiers":268},"Wu, 2004, 3D structure of human FK506-binding protein 52: Implications for the assembly of the glucocorticoid receptor\u002FHsp90\u002Fimmunophilin heterocomplex, Proc. Natl. Acad. Sci. USA, 101, 8348, 10.1073\u002Fpnas.0305969101",{"doi":269},"10.1073\u002Fpnas.0305969101",{"id":21,"text":271,"url":21,"identifiers":272},"Bracher, 2013, Crystal structures of the free and ligand-bound FK1-FK2 domain segment of FKBP52 reveal a flexible inter-domain hinge, J. Mol. Biol., 425, 4134, 10.1016\u002Fj.jmb.2013.07.041",{"doi":273},"10.1016\u002Fj.jmb.2013.07.041",{"id":21,"text":275,"url":21,"identifiers":276},"Marz, 2013, Large FK506-binding proteins shape the pharmacology of rapamycin, Mol. Cell. Biol., 33, 1357, 10.1128\u002FMCB.00678-12",{"doi":277},"10.1128\u002FMCB.00678-12",{"id":21,"text":279,"url":21,"identifiers":280},"Kozany, 2009, Fluorescent probes to characterise FK506-binding proteins, Chembiochem, 10, 1402, 10.1002\u002Fcbic.200800806",{"doi":281},"10.1002\u002Fcbic.200800806",{"id":21,"text":283,"url":21,"identifiers":284},"Wilson, 1995, Comparative X-ray structures of the major binding protein for the immunosuppressant FK506 (tacrolimus) in unliganded form and in complex with FK506 and rapamycin, Acta Crystallogr. D Biol. Crystallogr., 51, 511, 10.1107\u002FS0907444994014514",{"doi":285},"10.1107\u002FS0907444994014514",{"id":21,"text":287,"url":21,"identifiers":288},"Bracher, 2011, Structural characterization of the PPIase domain of FKBP51, a cochaperone of human Hsp90, Acta Crystallogr. D Biol. Crystallogr., 67, 549, 10.1107\u002FS0907444911013862",{"doi":289},"10.1107\u002FS0907444911013862",{"id":21,"text":291,"url":21,"identifiers":292},"Gopalakrishnan, 2012, Evaluation of synthetic FK506 analogues as ligands for the FK506-binding proteins 51 and 52, J. Med. Chem., 55, 4114, 10.1021\u002Fjm201746x",{"doi":293},"10.1021\u002Fjm201746x",{"id":21,"text":295,"url":21,"identifiers":296},"Wang, 2013, Increasing the efficiency of ligands for FK506-binding protein 51 by conformational control, J. Med. Chem., 56, 3922, 10.1021\u002Fjm400087k",{"doi":297},"10.1021\u002Fjm400087k",{"id":21,"text":299,"url":21,"identifiers":300},"Pomplun, 2018, Chemogenomic Profiling of Human and Microbial FK506-Binding Proteins, J. Med. Chem., 61, 3660, 10.1021\u002Facs.jmedchem.8b00137",{"doi":301},"10.1021\u002Facs.jmedchem.8b00137",{"id":21,"text":303,"url":21,"identifiers":304},"Gaali, 2015, Selective inhibitors of the FK506-binding protein 51 by induced fit, Nat. Chem. Biol., 11, 33, 10.1038\u002Fnchembio.1699",{"doi":305},"10.1038\u002Fnchembio.1699",{"id":21,"text":307,"url":21,"identifiers":308},"LeMaster, 2015, Coupling of Conformational Transitions in the N-terminal Domain of the 51-kDa FK506-binding Protein (FKBP51) Near Its Site of Interaction with the Steroid Receptor Proteins, J. Biol. Chem., 290, 15746, 10.1074\u002Fjbc.M115.650655",{"doi":309},"10.1074\u002Fjbc.M115.650655",{"id":21,"text":311,"url":21,"identifiers":312},"Mustafi, 2014, Differential conformational dynamics in the closely homologous FK506-binding domains of FKBP51 and FKBP52, Biochem. J., 461, 115, 10.1042\u002FBJ20140232",{"doi":313},"10.1042\u002FBJ20140232",{"id":21,"text":315,"url":21,"identifiers":316},"LeMaster, 2015, Conformational Dynamics in FKBP Domains: Relevance to Molecular Signaling and Drug Design, Curr. Mol. Pharmacol., 9, 5, 10.2174\u002F1874467208666150519113146",{"doi":317},"10.2174\u002F1874467208666150519113146",{"id":21,"text":319,"url":21,"identifiers":320},"Riggs, 2007, Noncatalytic role of the FKBP52 peptidyl-prolyl isomerase domain in the regulation of steroid hormone signaling, Mol. Cell. Biol., 27, 8658, 10.1128\u002FMCB.00985-07",{"doi":321},"10.1128\u002FMCB.00985-07",{"id":21,"text":323,"url":21,"identifiers":324},"Kumar, 2017, Combined X-ray crystallography and computational modeling approach to investigate the Hsp90 C-terminal peptide binding to FKBP51, Sci. Rep., 7, 14288, 10.1038\u002Fs41598-017-14731-z",{"doi":325},"10.1038\u002Fs41598-017-14731-z",{"id":21,"text":327,"url":21,"identifiers":328},"Scheufler, 2000, Structure of TPR domain-peptide complexes: Critical elements in the assembly of the Hsp70-Hsp90 multichaperone machine, Cell, 101, 199, 10.1016\u002FS0092-8674(00)80830-2",{"doi":329},"10.1016\u002FS0092-8674(00)80830-2",{"id":21,"text":331,"url":21,"identifiers":332},"Yang, J., Roe, S.M., Cliff, M.J., Williams, M.A., Ladbury, J.E., Cohen, P.T., and Barford, D. (2005). Molecular basis for TPR domain-mediated regulation of protein phosphatase 5. EMBO J.",{"doi":333},"10.1038\u002Fsj.emboj.7600496",{"id":21,"text":335,"url":21,"identifiers":336},"Blundell, K.L., Pal, M., Roe, S.M., Pearl, L.H., and Prodromou, C. (2017). The structure of FKBP38 in complex with the MEEVD tetratricopeptide binding-motif of Hsp90. PLoS ONE, 12.",{"doi":337},"10.1371\u002Fjournal.pone.0173543",{"id":21,"text":339,"url":21,"identifiers":340},"Ebong, 2016, The interchange of immunophilins leads to parallel pathways and different intermediates in the assembly of Hsp90 glucocorticoid receptor complexes, Cell Discov., 2, 16002, 10.1038\u002Fcelldisc.2016.2",{"doi":341},"10.1038\u002Fcelldisc.2016.2",{"id":21,"text":343,"url":21,"identifiers":344},"Assimon, 2015, Specific Binding of Tetratricopeptide Repeat Proteins to Heat Shock Protein 70 (Hsp70) and Heat Shock Protein 90 (Hsp90) Is Regulated by Affinity and Phosphorylation, Biochemistry, 54, 7120, 10.1021\u002Facs.biochem.5b00801",{"doi":345},"10.1021\u002Facs.biochem.5b00801",{"id":21,"text":347,"url":21,"identifiers":348},"Budzinski, 2016, The activity of the glucocorticoid receptor is regulated by SUMO conjugation to FKBP51, Cell Death Differ., 23, 1579, 10.1038\u002Fcdd.2016.44",{"doi":349},"10.1038\u002Fcdd.2016.44",{"id":21,"text":351,"url":21,"identifiers":352},"Roberts, 2003, C-terminal sequences outside the tetratricopeptide repeat domain of FKBP51 and FKBP52 cause differential binding to Hsp90, J. Biol. Chem., 278, 17388, 10.1074\u002Fjbc.M300955200",{"doi":353},"10.1074\u002Fjbc.M300955200",{"id":21,"text":355,"url":21,"identifiers":356},"Oroz, 2018, Structure and pro-toxic mechanism of the human Hsp90\u002FPPIase\u002FTau complex, Nat. Commun., 9, 4532, 10.1038\u002Fs41467-018-06880-0",{"doi":357},"10.1038\u002Fs41467-018-06880-0",{"id":21,"text":359,"url":21,"identifiers":360},"Zannas, 2016, Gene-Stress-Epigenetic Regulation of FKBP5: Clinical and Translational Implications, Neuropsychopharmacology, 41, 261, 10.1038\u002Fnpp.2015.235",{"doi":361},"10.1038\u002Fnpp.2015.235",{"id":21,"text":363,"url":21,"identifiers":364},"Matosin, 2018, Understanding the Molecular Mechanisms Underpinning Gene by Environment Interactions in Psychiatric Disorders: The FKBP5 Model, Biol. Psychiatry, 83, 821, 10.1016\u002Fj.biopsych.2018.01.021",{"doi":365},"10.1016\u002Fj.biopsych.2018.01.021",{"id":21,"text":367,"url":21,"identifiers":368},"Klengel, 2013, Allele-specific FKBP5 DNA demethylation mediates gene-childhood trauma interactions, Nat. Neurosci., 16, 33, 10.1038\u002Fnn.3275",{"doi":369},"10.1038\u002Fnn.3275",{"id":21,"text":371,"url":21,"identifiers":372},"Pereira, 2014, FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance, Metabolism, 63, 1198, 10.1016\u002Fj.metabol.2014.05.015",{"doi":373},"10.1016\u002Fj.metabol.2014.05.015",{"id":21,"text":375,"url":21,"identifiers":376},"Bortsov, 2013, Polymorphisms in the glucocorticoid receptor co-chaperone FKBP5 predict persistent musculoskeletal pain after traumatic stress exposure, Pain, 154, 1419, 10.1016\u002Fj.pain.2013.04.037",{"doi":377},"10.1016\u002Fj.pain.2013.04.037",{"id":21,"text":379,"url":21,"identifiers":380},"Linnstaedt, 2018, A Functional riboSNitch in the 3’ Untranslated Region of FKBP5 Alters MicroRNA-320a Binding Efficiency and Mediates Vulnerability to Chronic Post-Traumatic Pain, J. 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Chem., 58, 7796, 10.1021\u002Facs.jmedchem.5b00785",{"doi":719},"10.1021\u002Facs.jmedchem.5b00785",{"id":21,"text":721,"url":21,"identifiers":722},"Sidibeh, 2018, FKBP5 expression in human adipose tissue: Potential role in glucose and lipid metabolism, adipogenesis and type 2 diabetes, Endocrine, 62, 116, 10.1007\u002Fs12020-018-1674-5",{"doi":723},"10.1007\u002Fs12020-018-1674-5",false,{"id":726,"createTime":727,"updateTime":727,"relativeEntities":728,"slug":729,"properties":730,"entityType":124,"verifyStatus":125,"verifyTime":727,"verifyNote":126,"languages":745,"translateLanguages":21,"viewCount":22,"primaryUrl":746,"fullTextUrl":21,"authors":747,"publicationType":203,"publisherRelationship":811,"citationCount":864,"citationInfo":865,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":873,"openAccess":21,"references":874,"isForceReanalyzing":724},"30f5f1a4-ca7c-44ca-90eb-5f9848eff171","2025-02-11T03:17:06.273+00:00",[],"DOT1L-and-H3K79-Methylation-in-Transcription-and-Genomic-Stability",{"mag":731,"pmc":733,"openalex":735,"abstract":737,"title":739,"pm":741,"doi":743},{"VOID":732},"2791712220",{"VOID":734},"5871980",{"VOID":736},"W2791712220",{"EN":738},"\u003Cjats:p>The organization of eukaryotic genomes into chromatin provides challenges for the cell to accomplish basic cellular functions, such as transcription, DNA replication and repair of DNA damage. Accordingly, a range of proteins modify and\u002For read chromatin states to regulate access to chromosomal DNA. Yeast Dot1 and the mammalian homologue DOT1L are methyltransferases that can add up to three methyl groups to histone H3 lysine 79 (H3K79). H3K79 methylation is implicated in several processes, including transcription elongation by RNA polymerase II, the DNA damage response and cell cycle checkpoint activation. DOT1L is also an important drug target for treatment of mixed lineage leukemia (MLL)-rearranged leukemia where aberrant transcriptional activation is promoted by DOT1L mislocalisation. This review summarizes what is currently known about the role of Dot1\u002FDOT1L and H3K79 methylation in transcription and genomic stability.\u003C\u002Fjats:p>",{"EN":740},"DOT1L and H3K79 Methylation in Transcription and Genomic Stability",{"VOID":742},"29495487",{"VOID":744},"10.3390\u002Fbiom8010011",[128],"https:\u002F\u002Fwww.mdpi.com\u002F2218-273X\u002F8\u002F1\u002F11",[748,775,794],{"id":749,"sortIndex":22,"researcher":21,"roles":750,"affiliations":751,"properties":768,"displayName":772,"givenName":21,"familyName":21},"f6d5c30a-ee67-4461-bc34-6261f64e74f2",[],[752,760],{"id":753,"sortIndex":22,"affiliation":754,"properties":21},"8e57228d-5ec8-4688-8fc3-56563fe29046",{"id":753,"createTime":21,"updateTime":21,"relativeEntities":755,"slug":21,"properties":756,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":759,"statistic":21},[],{"title":757},{"EN":758},"Department of Biochemistry, 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Res., 762, 52, 10.1016\u002Fj.mrrev.2014.05.001",{"doi":1784},"10.1016\u002Fj.mrrev.2014.05.001",{"id":1786,"createTime":1787,"updateTime":1787,"relativeEntities":1788,"slug":1789,"properties":1790,"entityType":124,"verifyStatus":125,"verifyTime":1787,"verifyNote":126,"languages":1805,"translateLanguages":21,"viewCount":22,"primaryUrl":1806,"fullTextUrl":21,"authors":1807,"publicationType":203,"publisherRelationship":1867,"citationCount":871,"citationInfo":1920,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":1924,"openAccess":21,"references":1925,"isForceReanalyzing":724},"96964ca5-c594-4a42-828f-50b15771d19b","2025-02-01T11:23:22.179+00:00",[],"Thimet-Oligopeptidase-Biochemical-and-Biological-Significances-Past-Present-and-Future-Directions",{"mag":1791,"pmc":1793,"openalex":1795,"abstract":1797,"title":1799,"pm":1801,"doi":1803},{"VOID":1792},"3080782276",{"VOID":1794},"7565970",{"VOID":1796},"W3080782276",{"EN":1798},"\u003Cjats:p>Thimet oligopeptidase (EC 3.4.24.15; EP24.15, THOP1) is a metallopeptidase ubiquitously distributed in mammalian tissues. Beyond its previously well characterized role in major histocompatibility class I (MHC-I) antigen presentation, the recent characterization of the THOP1 C57BL6\u002FN null mice (THOP1−\u002F−) phenotype suggests new key functions for THOP1 in hyperlipidic diet-induced obesity, insulin resistance and non-alcoholic liver steatosis. Distinctive levels of specific intracellular peptides (InPeps), genes and microRNAs were observed when comparing wild type C57BL6\u002FN to THOP1−\u002F− fed either standard or hyperlipidic diets. A possible novel mechanism of action was suggested for InPeps processed by THOP1, which could be modulating protein-protein interactions and microRNA processing, thus affecting the phenotype. Together, research into the biochemical and biomedical significance of THOP1 suggests that degradation by the proteasome is a step in the processing of various proteins, not merely for ending their existence. This allows many functional peptides to be generated by proteasomal degradation in order to, for example, control mRNA translation and the formation of protein complexes.\u003C\u002Fjats:p>",{"EN":1800},"Thimet Oligopeptidase Biochemical and Biological Significances: Past, Present, and Future Directions",{"VOID":1802},"32847123",{"VOID":1804},"10.3390\u002Fbiom10091229",[128],"https:\u002F\u002Fwww.mdpi.com\u002F2218-273X\u002F10\u002F9\u002F1229",[1808,1835,1850],{"id":1809,"sortIndex":22,"researcher":21,"roles":1810,"affiliations":1811,"properties":1828,"displayName":1832,"givenName":21,"familyName":21},"8beef5c6-e1f2-45c9-a048-6a38034e92d2",[],[1812,1820],{"id":1813,"sortIndex":22,"affiliation":1814,"properties":21},"5fa067f3-0f1d-40bc-82cd-8a33ac17aa9b",{"id":1813,"createTime":21,"updateTime":21,"relativeEntities":1815,"slug":21,"properties":1816,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":1819,"statistic":21},[],{"title":1817},{"VI":1818},"Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 7610001, Israel",[],{"id":1821,"sortIndex":150,"affiliation":1822,"properties":21},"699ce7cf-4779-46ba-b89c-459913671b3d",{"id":1821,"createTime":21,"updateTime":21,"relativeEntities":1823,"slug":21,"properties":1824,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":1827,"statistic":21},[],{"title":1825},{"EN":1826},"Pharmacology Department, Biomedical Science Institute, University of São Paulo, São Paulo, SP 05508-000, Brazil",[],{"orcid":1829,"title":1831,"openalex":1833},{"VOID":1830},"https:\u002F\u002Forcid.org\u002F0000-0003-1651-9192",{"EN":1832},"Emer S. 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Dis., 182, 214, 10.1086\u002F315682",{"doi":2545},"10.1086\u002F315682",{"id":21,"text":2547,"url":21,"identifiers":2548},"Singer, 2016, The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3), JAMA, 315, 801, 10.1001\u002Fjama.2016.0287",{"doi":2549},"10.1001\u002Fjama.2016.0287",{"id":21,"text":2551,"url":21,"identifiers":2552},"Orlowski, 1988, Substrate-related potent inhibitors of brain metalloendopeptidase, Biochemistry, 27, 597, 10.1021\u002Fbi00402a015",{"doi":2553},"10.1021\u002Fbi00402a015",{"id":21,"text":2555,"url":21,"identifiers":2556},"Cardozo, 1993, Evidence that enzymatic conversion of N-[1(R,S)-carboxy-3-phenylpropyl]-Ala-Ala-Phe-p-aminobenzoate, a specific inhibitor of endopeptidase 24.15, to N-[1(R,S)-carboxy-3-phenylpropyl]-Ala-Ala is necessary for inhibition of angiotensin converting enzyme, Peptides, 14, 1259, 10.1016\u002F0196-9781(93)90185-J",{"doi":2557},"10.1016\u002F0196-9781(93)90185-J",{"id":21,"text":2559,"url":21,"identifiers":2560},"Lew, 2000, Bradykinin analogues with beta-amino acid substitutions reveal subtle differences in substrate specificity between the endopeptidases EC 3.4.24.15 and EC 3.4.24.16, J. 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Sci. Transl. Med., 12.",{"doi":2573},"10.1126\u002Fscitranslmed.aaz8264",{"id":21,"text":2575,"url":21,"identifiers":2576},"Goh, 2007, The human disease network, Proc. Natl. Acad. Sci. USA, 104, 8685, 10.1073\u002Fpnas.0701361104",{"doi":2577},"10.1073\u002Fpnas.0701361104",{"id":21,"text":2579,"url":21,"identifiers":2580},"Vidal, 2011, Interactome networks and human disease, Cell, 144, 986, 10.1016\u002Fj.cell.2011.02.016",{"doi":2581},"10.1016\u002Fj.cell.2011.02.016",{"id":21,"text":2583,"url":21,"identifiers":2584},"Menche, 2015, Disease networks. Uncovering disease-disease relationships through the incomplete interactome, Science, 347, 1257601, 10.1126\u002Fscience.1257601",{"doi":2585},"10.1126\u002Fscience.1257601",{"id":21,"text":2587,"url":21,"identifiers":2588},"Kovacs, 2019, Network-based prediction of protein interactions, Nat. Commun., 10, 1240, 10.1038\u002Fs41467-019-09177-y",{"doi":2589},"10.1038\u002Fs41467-019-09177-y",{"id":21,"text":2591,"url":21,"identifiers":2592},"The Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium (2011). Genome-wide association study identifies five new schizophrenia loci. Nat. Genet., 43, 969–976.",{"doi":2593},"10.1038\u002Fng.940",{"id":2595,"createTime":2596,"updateTime":2596,"relativeEntities":2597,"slug":2598,"properties":2599,"entityType":124,"verifyStatus":125,"verifyTime":2596,"verifyNote":126,"languages":2614,"translateLanguages":21,"viewCount":22,"primaryUrl":2615,"fullTextUrl":21,"authors":2616,"publicationType":203,"publisherRelationship":2741,"citationCount":2794,"citationInfo":2795,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":2800,"openAccess":21,"references":2801,"isForceReanalyzing":724},"d594d433-f4be-4c7e-9885-291d01cd12c2","2025-02-01T11:23:21.283+00:00",[],"Intracellular-Peptides-in-Cell-Biology-and-Pharmacology",{"mag":2600,"pmc":2602,"openalex":2604,"abstract":2606,"title":2608,"pm":2610,"doi":2612},{"VOID":2601},"2936512562",{"VOID":2603},"6523763",{"VOID":2605},"W2936512562",{"EN":2607},"\u003Cjats:p>Intracellular peptides are produced by proteasomes following degradation of nuclear, cytosolic, and mitochondrial proteins, and can be further processed by additional peptidases generating a larger pool of peptides within cells. Thousands of intracellular peptides have been sequenced in plants, yeast, zebrafish, rodents, and in human cells and tissues. Relative levels of intracellular peptides undergo changes in human diseases and also when cells are stimulated, corroborating their biological function. However, only a few intracellular peptides have been pharmacologically characterized and their biological significance and mechanism of action remains elusive. Here, some historical and general aspects on intracellular peptides’ biology and pharmacology are presented. Hemopressin and Pep19 are examples of intracellular peptides pharmacologically characterized as inverse agonists to cannabinoid type 1 G-protein coupled receptors (CB1R), and hemopressin fragment NFKF is shown herein to attenuate the symptoms of pilocarpine-induced epileptic seizures. Intracellular peptides EL28 (derived from proteasome 26S protease regulatory subunit 4; Rpt2), PepH (derived from Histone H2B type 1-H), and Pep5 (derived from G1\u002FS-specific cyclin D2) are examples of peptides that function intracellularly. Intracellular peptides are suggested as biological functional molecules, and are also promising prototypes for new drug development.\u003C\u002Fjats:p>",{"EN":2609},"Intracellular Peptides in Cell Biology and Pharmacology",{"VOID":2611},"30995799",{"VOID":2613},"10.3390\u002Fbiom9040150",[128],"https:\u002F\u002Fwww.mdpi.com\u002F2218-273X\u002F9\u002F4\u002F150",[2617,2636,2653,2670,2689,2708,2725],{"id":2618,"sortIndex":22,"researcher":21,"roles":2619,"affiliations":2620,"properties":2629,"displayName":2633,"givenName":21,"familyName":21},"ed0e92b6-6fdd-414b-876c-e1e7b82cf45e",[],[2621],{"id":2622,"sortIndex":22,"affiliation":2623,"properties":21},"b0916968-4816-4c29-b4f7-27025ba500bd",{"id":2622,"createTime":21,"updateTime":21,"relativeEntities":2624,"slug":21,"properties":2625,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":2628,"statistic":21},[],{"title":2626},{"EN":2627},"Special Laboratory of Cell Cycle, Center of Toxins, Immune Response and Cell Signaling—CeTICS, Butantan Institute, São Paulo SP 05503-900, Brazil",[],{"orcid":2630,"title":2632,"openalex":2634},{"VOID":2631},"https:\u002F\u002Forcid.org\u002F0000-0002-6801-4367",{"EN":2633},"Christiane B. de Araujo",{"VOID":2635},"A5042116796",{"id":2637,"sortIndex":150,"researcher":21,"roles":2638,"affiliations":2639,"properties":2648,"displayName":2650,"givenName":21,"familyName":21},"1a82b630-d625-4ca3-8941-aa5db9ad4b5b",[],[2640],{"id":2641,"sortIndex":22,"affiliation":2642,"properties":21},"a74f4a4c-f85f-4993-93bc-4c1fbf8464df",{"id":2641,"createTime":21,"updateTime":21,"relativeEntities":2643,"slug":21,"properties":2644,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":2647,"statistic":21},[],{"title":2645},{"EN":2646},"Proteimax Biotecnologia LTDA, São Paulo SP 05581-001, Brazil",[],{"title":2649,"openalex":2651},{"EN":2650},"Andrea S. 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2005, Neuropeptide-processing enzymes: Applications for drug discovery, AAPS J., 7, E449, 10.1208\u002Faapsj070244",{"doi":2805},"10.1208\u002Faapsj070244",{"id":21,"text":2807,"url":21,"identifiers":2808},"Glickman, 2002, The ubiquitin-proteasome proteolytic pathway: Destruction for the sake of construction, Physiol. Rev., 82, 373, 10.1152\u002Fphysrev.00027.2001",{"doi":2809},"10.1152\u002Fphysrev.00027.2001",{"id":21,"text":2811,"url":21,"identifiers":2812},"Dolan, 2011, Translating DRiPs: Progress in understanding viral and cellular sources of MHC class I peptide ligands, Cell. Mol. Life Sci., 68, 1481, 10.1007\u002Fs00018-011-0656-z",{"doi":2813},"10.1007\u002Fs00018-011-0656-z",{"id":21,"text":2815,"url":21,"identifiers":2816},"Lee, 2015, The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance, Cell Metab., 21, 443, 10.1016\u002Fj.cmet.2015.02.009",{"doi":2817},"10.1016\u002Fj.cmet.2015.02.009",{"id":21,"text":2819,"url":21,"identifiers":2820},"Rist, 2013, HLA peptide length preferences control CD8+ T cell responses, J. Immunol., 191, 561, 10.4049\u002Fjimmunol.1300292",{"doi":2821},"10.4049\u002Fjimmunol.1300292",{"id":21,"text":2823,"url":21,"identifiers":2824},"Burrows, 2008, Preferential binding of unusually long peptides to MHC class I and its influence on the selection of target peptides for T cell recognition, Mol. Immunol., 45, 1818, 10.1016\u002Fj.molimm.2007.09.026",{"doi":2825},"10.1016\u002Fj.molimm.2007.09.026",{"id":21,"text":2827,"url":21,"identifiers":2828},"Kloverpris, 2013, HLA-specific intracellular epitope processing shapes an immunodominance pattern for HLA-B*57 that is distinct from HLA-B*58:01, J. Virol., 87, 10889, 10.1128\u002FJVI.01122-13",{"doi":2829},"10.1128\u002FJVI.01122-13",{"id":21,"text":2831,"url":21,"identifiers":2832},"Caron, 2015, Analysis of Major Histocompatibility Complex (MHC) Immunopeptidomes Using Mass Spectrometry, Mol. Cell. Proteom., 14, 3105, 10.1074\u002Fmcp.O115.052431",{"doi":2833},"10.1074\u002Fmcp.O115.052431",{"id":21,"text":2835,"url":21,"identifiers":2836},"Connell, 1957, Intracellular peptides of Pseudomonas hydrophila, Biochim. Biophys. Acta, 24, 226, 10.1016\u002F0006-3002(57)90184-1",{"doi":2837},"10.1016\u002F0006-3002(57)90184-1",{"id":21,"text":2839,"url":21,"identifiers":2840},"McManus, 1958, Synthesis of intracellular peptides in Torula utilis, J. Biol. Chem., 231, 777, 10.1016\u002FS0021-9258(18)70441-9",{"doi":2841},"10.1016\u002FS0021-9258(18)70441-9",{"id":21,"text":2843,"url":21,"identifiers":2844},"Guidotti, 1983, Isolation, characterization, and purification to homogeneity of an endogenous polypeptide with agonistic action on benzodiazepine receptors, Proc. Natl. Acad. Sci. USA, 80, 3531, 10.1073\u002Fpnas.80.11.3531",{"doi":2845},"10.1073\u002Fpnas.80.11.3531",{"id":21,"text":2847,"url":21,"identifiers":2848},"Alho, 1985, Diazepam-binding inhibitor: A neuropeptide located in selected neuronal populations of rat brain, Science, 229, 179, 10.1126\u002Fscience.3892688",{"doi":2849},"10.1126\u002Fscience.3892688",{"id":21,"text":2851,"url":21,"identifiers":2852},"Huyer, 2006, Saccharomyces cerevisiae a-factor mutants reveal residues critical for processing, activity, and export, Eukaryot. Cell, 5, 1560, 10.1128\u002FEC.00161-06",{"doi":2853},"10.1128\u002FEC.00161-06",{"id":21,"text":1975,"url":21,"identifiers":2855},{"doi":1977},{"id":21,"text":2857,"url":21,"identifiers":2858},"Rioli, 2018, Substrate Capture Assay Using Inactive Oligopeptidases to Identify Novel Peptides, Methods Mol. 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Commun., 10, 329, 10.1038\u002Fs41467-018-08276-6",{"doi":3342},"10.1038\u002Fs41467-018-08276-6",{"id":3344,"createTime":3345,"updateTime":3345,"relativeEntities":3346,"slug":3347,"properties":3348,"entityType":124,"verifyStatus":125,"verifyTime":3345,"verifyNote":126,"languages":3363,"translateLanguages":21,"viewCount":22,"primaryUrl":3364,"fullTextUrl":21,"authors":3365,"publicationType":203,"publisherRelationship":3431,"citationCount":869,"citationInfo":3484,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":3486,"openAccess":21,"references":3487,"isForceReanalyzing":724},"9e2ebefd-6892-4578-96aa-2739dfe449e9","2025-01-29T08:56:45.476+00:00",[],"Medical-Therapy-of-Patients-Contaminated-with-Radioactive-Cesium-or-Iodine",{"mag":3349,"pmc":3351,"openalex":3353,"abstract":3355,"title":3357,"pm":3359,"doi":3361},{"VOID":3350},"2996399409",{"VOID":3352},"6995530",{"VOID":3354},"W2996399409",{"EN":3356},"\u003Cjats:p>Follow-up studies after the Chernobyl and Fukushima accidents have shown that 137Cs and 131I made up the major amount of harmful contaminants in the atmospheric dispersion and fallout. Other potential sources for such radionuclide exposure may be terrorist attacks, e.g., via contamination of drinking water reservoirs. A primary purpose of radionuclide mobilization is to minimize the radiation dose. Rapid initiation of treatment of poisoned patients is imperative after a contaminating event. Internal contamination with radioactive material can expose patients to prolonged radiation, thus leading to short- and long-term clinical consequences. After the patient’s emergency conditions are addressed, the treating physicians and assisting experts should assess the amount of radioactive material that has been internalized. This evaluation should include estimation of the radiation dose that is delivered and the specific radionuclides inside the body. These complex assessments warrant the reliance on a multidisciplinary approach that incorporates regional experts in radiation medicine and emergencies. Regional hospitals should have elaborated strategies for the handling of radiation emergencies. If radioactive cesium is a significant pollutant, Prussian blue is the approved antidote for internal detoxification. Upon risks of radioiodine exposure, prophylactic or immediate treatment with potassium iodide tablets is recommended. 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Medical Effectiveness of Iodine Prophylaxis in a Nuclear Reactor Emergency Situation and Overview of European Practices. Available online: https:\u002F\u002Fec.europa.eu\u002Fenergy\u002Fsites\u002Fener\u002Ffiles\u002Fdocuments\u002F165.pdf.",{},{"id":21,"text":3606,"url":21,"identifiers":3607},"Kowalsky, R.J., and Falen, S.W. (2011). Radiopharmaceuticals in Nuclear Pharmacy and Nuclear Medicine, American Pharmacists Association.",{},{"id":21,"text":3609,"url":21,"identifiers":3610},"Law, 2013, National surveillance for radiological exposures and intentional potassium iodide and iodine product ingestions in the United States associated with the 2011 Japan radiological incident, Clin. Toxicol., 51, 41, 10.3109\u002F15563650.2012.732701",{"doi":3611},"10.3109\u002F15563650.2012.732701",{"id":21,"text":3613,"url":21,"identifiers":3614},"Aaseth, J., Crisponi, G., and Andersen, O. (2016). 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Res., 28, 212, 10.1002\u002Fptr.4981",{"doi":4143},"10.1002\u002Fptr.4981",{"id":4145,"createTime":4146,"updateTime":4146,"relativeEntities":4147,"slug":4148,"properties":4149,"entityType":124,"verifyStatus":125,"verifyTime":4146,"verifyNote":126,"languages":4164,"translateLanguages":21,"viewCount":22,"primaryUrl":4165,"fullTextUrl":21,"authors":4166,"publicationType":203,"publisherRelationship":4231,"citationCount":4284,"citationInfo":4285,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":4291,"openAccess":21,"references":4292,"isForceReanalyzing":724},"8b7eafbb-c117-4155-9f56-70e8c6dc65a7","2025-01-28T19:34:39.134+00:00",[],"MYC-Driven-Pathways-in-Breast-Cancer-Subtypes",{"mag":4150,"pmc":4152,"openalex":4154,"abstract":4156,"title":4158,"pm":4160,"doi":4162},{"VOID":4151},"2734462584",{"VOID":4153},"5618234",{"VOID":4155},"W2734462584",{"EN":4157},"\u003Cjats:p>The transcription factor MYC (MYC proto-oncogene, bHLH transcription factor) is an essential signaling hub in multiple cellular processes that sustain growth of many types of cancers. MYC regulates expression of RNA, both protein and non-coding, that control central metabolic pathways, cell death, proliferation, differentiation, stress pathways, and mechanisms of drug resistance. Activation of MYC has been widely reported in breast cancer progression. Breast cancer is a complex heterogeneous disease and treatment options are primarily guided by histological and biochemical evaluations of the tumors. Based on biochemical markers, three main breast cancer categories are ER+ (estrogen receptor alpha positive), HER2+ (human epidermal growth factor receptor 2 positive), and TNBC (triple-negative breast cancer; estrogen receptor negative, progesterone receptor negative, HER2 negative). MYC is elevated in TNBC compared with other cancer subtypes. Interestingly, MYC-driven pathways are further elevated in aggressive breast cancer cells and tumors that display drug resistant phenotype. Identification of MYC target genes is essential in isolating signaling pathways that drive tumor development. In this review, we address the role of MYC in the three major breast cancer subtypes and highlight the most promising leads to target MYC functions.\u003C\u002Fjats:p>",{"EN":4159},"MYC-Driven Pathways in Breast Cancer Subtypes",{"VOID":4161},"28696357",{"VOID":4163},"10.3390\u002Fbiom7030053",[128],"https:\u002F\u002Fwww.mdpi.com\u002F2218-273X\u002F7\u002F3\u002F53",[4167,4184,4199,4214],{"id":4168,"sortIndex":22,"researcher":21,"roles":4169,"affiliations":4170,"properties":4179,"displayName":4181,"givenName":21,"familyName":21},"1bd4cf77-755f-45db-8ee6-ccfb07ec9ddd",[],[4171],{"id":4172,"sortIndex":22,"affiliation":4173,"properties":21},"c07826cc-ff3c-4e05-80e8-4e91a594aedc",{"id":4172,"createTime":21,"updateTime":21,"relativeEntities":4174,"slug":21,"properties":4175,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":4178,"statistic":21},[],{"title":4176},{"VI":4177},"Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA",[],{"title":4180,"openalex":4182},{"EN":4181},"Yassi Fallah",{"VOID":4183},"A5063718690",{"id":4185,"sortIndex":150,"researcher":21,"roles":4186,"affiliations":4187,"properties":4194,"displayName":4196,"givenName":21,"familyName":21},"abaf211b-b556-4ae7-9931-5fdb4c7bc0e6",[],[4188],{"id":4172,"sortIndex":22,"affiliation":4189,"properties":21},{"id":4172,"createTime":21,"updateTime":21,"relativeEntities":4190,"slug":21,"properties":4191,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":4193,"statistic":21},[],{"title":4192},{"VI":4177},[],{"title":4195,"openalex":4197},{"EN":4196},"Janetta Brundage",{"VOID":4198},"A5114173869",{"id":4200,"sortIndex":166,"researcher":21,"roles":4201,"affiliations":4202,"properties":4209,"displayName":4211,"givenName":21,"familyName":21},"33e01eca-fe1e-433c-8f1e-9f3ddfdbfb1b",[],[4203],{"id":4172,"sortIndex":22,"affiliation":4204,"properties":21},{"id":4172,"createTime":21,"updateTime":21,"relativeEntities":4205,"slug":21,"properties":4206,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":4208,"statistic":21},[],{"title":4207},{"VI":4177},[],{"title":4210,"openalex":4212},{"EN":4211},"Paul Allegakoen",{"VOID":4213},"A5022697592",{"id":4215,"sortIndex":90,"researcher":21,"roles":4216,"affiliations":4217,"properties":4224,"displayName":4228,"givenName":21,"familyName":21},"d96e8525-1b75-4cd8-9872-97e67df26455",[],[4218],{"id":4172,"sortIndex":22,"affiliation":4219,"properties":21},{"id":4172,"createTime":21,"updateTime":21,"relativeEntities":4220,"slug":21,"properties":4221,"entityType":21,"verifyStatus":21,"verifyTime":21,"verifyNote":21,"languages":21,"translateLanguages":21,"viewCount":21,"url":21,"parentIds":4223,"statistic":21},[],{"title":4222},{"VI":4177},[],{"orcid":4225,"title":4227,"openalex":4229},{"VOID":4226},"https:\u002F\u002Forcid.org\u002F0000-0001-7616-320X",{"EN":4228},"Ayesha N. 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Health Perspect., 124, 563, 10.1289\u002Fehp.1409200",{"doi":4475},"10.1289\u002Fehp.1409200",{"id":4477,"createTime":4478,"updateTime":4478,"relativeEntities":4479,"slug":4480,"properties":4481,"entityType":124,"verifyStatus":125,"verifyTime":4478,"verifyNote":126,"languages":4496,"translateLanguages":21,"viewCount":22,"primaryUrl":4497,"fullTextUrl":21,"authors":4498,"publicationType":203,"publisherRelationship":4537,"citationCount":4589,"citationInfo":4590,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":4596,"openAccess":21,"references":4597,"isForceReanalyzing":724},"7429fd37-2f0b-4c86-ac0c-55cddef673a4","2025-01-01T21:30:29.253+00:00",[],"Impact-of-Oxidative-Stress-on-Exercising-Skeletal-Muscle",{"mag":4482,"pmc":4484,"openalex":4486,"abstract":4488,"title":4490,"pm":4492,"doi":4494},{"VOID":4483},"2037055992",{"VOID":4485},"4496677",{"VOID":4487},"W2037055992",{"EN":4489},"\u003Cjats:p>It is well established that muscle contractions during exercise lead to elevated levels of reactive oxygen species (ROS) in skeletal muscle. These highly reactive molecules have many deleterious effects, such as a reduction of force generation and increased muscle atrophy. Since the discovery of exercise-induced oxidative stress several decades ago, evidence has accumulated that ROS produced during exercise also have positive effects by influencing cellular processes that lead to increased expression of antioxidants. These molecules are particularly elevated in regularly exercising muscle to prevent the negative effects of ROS by neutralizing the free radicals. In addition, ROS also seem to  be involved in the exercise-induced adaptation of the muscle phenotype. This review provides an overview of the evidences to date on the effects of ROS in exercising muscle. These aspects include the sources of ROS, their positive and negative cellular effects, the role of antioxidants, and the present evidence on ROS-dependent adaptations of muscle cells  in response to physical exercise.\u003C\u002Fjats:p>",{"EN":4491},"Impact of Oxidative Stress on Exercising Skeletal 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