<HashMap><database>MassIVE</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://massive-ftp.ucsd.edu/v01/MSV000079437/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>0</viewCount><searchCount>0</searchCount></scores><additional><omics_type>Proteomics</omics_type><submitter>Lijun Zhong, Juntuo Zhou, Yuxin Yin, Yan Pan</submitter><instrument_platform>LTQ Orbitrap Velos</instrument_platform><species>Homo Sapiens (ncbitaxon:9606)</species><full_dataset_link>https://massive.ucsd.edu/ProteoSAFe/dataset.jsp?task=6a43a3051000430fa984d79f27112ac1</full_dataset_link><sample_protocol></sample_protocol><repository>MassIVE</repository><file_size>85</file_size><ptm_modification>MS:1002864 - No post-translational-modifications are included in the identified peptides of this dataset</ptm_modification><data_protocol></data_protocol><pubmed_abstract>B12 belongs to the coumarin class of compounds that have been shown to have various physiological and pharmacological activities including anti-inflammatory, antibacterial, and antioxidant. In the present study, we characterised the neuroprotective effects of B12 against H2O2-induced neuronal cell damage in SH-SY5Y cells. Protein expression profiling in combination with pathway analysis was deployed to investigate the molecular events associated with the neuroprotective effects in human neuronal cells using a label-free quantitative proteomics approach. A total of 22 proteins were significantly differentially expressed in H2O2-damaged cells with or without B12 treatment. Bioinformatics analysis using the Cytoscape platform indicated that poly pyrimidine tract binding protein 1 (PTBP1) was highly associated with the protective effect, and western blotting verified that PTBP1 was up-regulated in H2O2 + B12 treatment group, compared with the H2O2 treated group. PTBP RNAi experiments knocked down PTBP expression, which cancelled out the protective effect of B12 on cell viability. Thus, we infer that B12 neuroprotective activity involves up-regulation of PTBP1 and its associated signalling networks following H2O2-induced apoptosis in SH-SY5Y cells. B12 or related compounds may prove to be useful therapeutic agents for the treatment of neurodegenerative diseases such as Alzheimer's and Parkinson's.</pubmed_abstract><pubmed_title>Quantitative proteomics study of the neuroprotective effects of B12 on hydrogen peroxide-induced apoptosis in SH-SY5Y cells.</pubmed_title><pubmed_authors>Zhong Lijun L, Zhou Juntuo J, Chen Xi X, Lou Yaxin Y, Liu Dan D, Zou Xiajuan X, Yang Bin B, Yin Yuxin Y, Pan Yan Y</pubmed_authors><pubmed_title_synonyms>EDP1, SHSY5Y, SH-SY5Y, study, hydrogen peroxide-induced apoptosis, B12, count in organism, intrinsic apoptotic signaling pathway in response to H2O2, Peptidomics, BTBD34, hydrogen peroxide-induced intrinsic apoptotic signaling pathway, number, CI-B12, Cell., presence, H2O2-induced intrinsic apoptotic signaling pathway, B61, hBACURD2</pubmed_title_synonyms><pubmed_abstract_synonyms>SH-SY5Y, Anti Oxidants, Tonka bean camphor, Presenile Alzheimer Dementia, ALZHEIMERS DIS, Activity, determination, H2O2, Parkinson's disease NOS, Pybp, Oxydol, Neurologic Diseases, protein, Neurologic Degenerative Condition, Viabilities, type I programmed cell death, dihydrogen dioxide, axonal tract, IDIOPATHIC PARKINSON DIS, Alzheimer's disease, MAGE-E1 antigen, Neurodegenerative Diseases, AD, 6-Benzo-2-pyrone, protein polypeptide chains, neutrophilic leucocyte, AL033359, Extrinsic Pathway Apoptoses, Neurologic Disorders, BTBD34, Programmed, neutrophil leukocyte, Post Transcriptional, 1, delta-lactone, 5, d-lactone, protein aggregate, Viability, Nervous System Degenerative Diseases, Presenile Alzheimer, treatment, Anti Oxidant, perhydrol, Pybp2, Pybp1, Degenerative Condition, Parkinsons disease, Man (Taxonomy), Parkinson disease, DAT - Dementia Alzheimer's type, Parkinson's disease (disorder), 2-Benzopyrone, proteins, quelling, Neurodegenerative Disorder, free, set, Gene Silencings, Intrinsic Pathway Apoptosis, 2H-1-Benzopyran-2-one, Degenerative Neurologic Disease, HCA1, AD - Alzheimer's disease, Classic, Antioxidant, PTB-1, signaling process, polymorphonuclear leukocyte, polynuclear neutrophilic leucocyte, Alzheimer Type Dementia, Classical Apoptosis, Anti-Oxidant Effect, disease management, Therapies, Neurologic Degenerative Disease, Parkinson syndrome, HNRNPI, associated, Presenile, pPTB, Alzheimers disease, B61, single organism signaling, Parkinson's syndrome, Therapy, cellular suicide, Parkinsons, tract of neuraxis, sporadic Alzheimer's disease, Caspase-Dependent Apoptosis, Modern, Antioxidants, PARKINSON DIS, Up-Regulation (Physiology), Endogenous, PARKINSON DIS IDIOPATHIC, Anti-Oxidants, hnrnp-I, Alzheimer's Dementia, AA407203, Alzheimer Type, neutrocyte, Idiopathic Parkinson's Disease, signaling (initiator) caspase activity, induction of apoptosis, Intrinsic Pathway, Lewy Body Parkinson Disease, Extrinsic Pathway Apoptosis, DAMAGE, Hepatocellular carcinoma-associated protein 1, NOS, nerve tract, PARKINSONS DIS LEWY BODY., Caspase-Dependent, RNA Silencing, vgrbp60, Post-Transcriptional Gene, PTB, Ptb, Dementia, SHSY5Y, antioxidants, Alzheimers, hnrpi, Benzo-alpha-pyrone, Degenerative Diseases, Upregulation, Alzheimer, 6-benzo-alpha-pyrone, Cell Death, Neurologic Disease, Co Suppression, Treatments, human, Post Transcriptional Gene Silencing, ptb, Alzheimer's, EDP1, Intrinsic Pathway Apoptoses, Endogenous Antioxidants, Gene Silencing, induction of apoptosis by p53, Degenerative, label, PARKINSONS DIS IDIOPATHIC, Extrinsic Pathway, Co-Suppression, mMage-e1, Classical, Apoptoses, 2-benzopyrone, Gruppe, Dementia of the Alzheimer's type, HOOH, polynuclear neutrophilic leukocyte, post-transcriptional gene silencing by RNA, 2-Propenoic acid, biological signaling, nerve cell, human being, 3-(2-hydroxyphenyl)-, Peptidomics, Endogenous Antioxidant, Lewy Body, 2H-benzo[b]pyran-2-one, antoxidant, PTB3, caspase-dependent programmed cell death, number, PTB2, PTB4, Degenerative Neurologic Disorders, antioxydant, Gene, Caspase Dependent Apoptosis, o-Hydroxycinnamic acid lactone, protein-containing complex, apoptotic programmed cell death, presence, activation of apoptosis, cerebral degeneration disease, HNRPI, unspecified (disorder), Human, ALZHEIMER DIS, polypeptide chain, Homo sapiens, [X]Dementia in Alzheimer's disease, Anti-Oxidant, Survival, Gene Products, Anti-Oxidant Effects, Type I, Coumarine, Man, neuraxis tract, study, Nervous System, Receptor Up-Regulation, ligand, neutrophil leucocyte, Up Regulation, o-hydroxycinnamic acid delta-lactone, cis-o-Coumarinic acid lactone, AI847422, neutrophilic leukocyte, IDIOPATHIC PARKINSONS DIS, apoptosis activator activity, man, Cosuppression, Neurodegenerative Disorders, Idiopathic PD, Parkinson's, Neurologic, Neurologic Degenerative Diseases, Idiopathic, grupos, Classic Apoptosis, Alzheimer Disease, Antioxidant Activity, [OH(OH)], execution phase of apoptotic process, Degenerative Neurologic Diseases, Parkinson Disease, Parkinsonism, PARKINSONS DIS, Spinal Cord, Alzheimer's disease (disorder), Rattex, programmed cell death by apoptosis, Alzheimers Dementia, ptbp1, Apoptosis, RNA, Disease, Primary Parkinsonism, Neurologic Disorder, cell suicide, HNRNP-I, grupo, PTB-T, Coumarinic anhydride, protein complex, Alpha-dystrobrevin-associated MAGE Protein, Proteins, apoptotic cell death, posttranscriptional gene silencing by siRNA, CI-B12, Paralysis agitans, Primary, cosuppression, Anti Oxidant Effect, Cell, group, Idiopathic Parkinson Disease, LEWY BODY PARKINSON DIS, Cell Viabilities, Degenerative Neurologic Disorder, [X]Dementia in Alzheimer's disease (disorder), RNAi, count in organism, Cumarin, Interference, native protein, natural protein, Parkinson's Disease, Antioxidant Effect, Programmed Cell Death, Protein, chemical analysis, Benzo-a-pyrone, Silencing, Post-Transcriptional Gene Silencings, apoptosis signaling, Anti Oxidant Effects, Degenerative Conditions, tract, apoptosis, ensemble, RGD1560259, Posttranscriptional, Dementia in Alzheimer's disease, Posttranscriptional Gene Silencing, Rest, Neurologic Degenerative Conditions, Alzheimer Dementia, signalling, hBACURD2, Lewy Body Parkinson's Disease, Protein Gene Products, Classic Apoptoses, Parkinsonian disorder, Antioxidant Effects, Gene Proteins, B12, Post-Transcriptional, neuronal cell, signalling process, Therapeutic, Parkinson's disease NOS (disorder), apoptotic program, Modern Man, Dementia in Alzheimer's disease (disorder), PMN, commitment to apoptosis, polymorphonuclear leucocyte, Neurodegenerative Disease, Treatment, Central Nervous System, assay, poly, Post-Transcriptional Gene Silencing, Cell Viability, groupe, General activity, polymorphonuclear neutrophil</pubmed_abstract_synonyms><name_synonyms>liquid chromatography tandem mass spectroscopy, LC-MS2, EDP1, SHSY5Y, SH-SY5Y, B12, LC/MS/MS, LCMSMS, determination, liquid chromatography-tandem mass spectroscopy, BTBD34, LC-MSMS, chemical analysis, LC-MS/MS, liquid chromatography tandem mass spectrometry, CI-B12, Cell., assay, B61, LC-MS-MS, hBACURD2</name_synonyms><description_synonyms>SHSY5Y, Peptidomics., SH-SY5Y, human being, Man (Taxonomy), protein complex, Modern, Proteins, number, CI-B12, Gene, proteins, protein, protein-containing complex, man, free, presence, human, Cell, hBACURD2, EDP1, Protein Gene Products, Human, Gene Proteins, B12, protein polypeptide chains, count in organism, native protein, natural protein, polypeptide chain, Homo sapiens, BTBD34, label, Modern Man, Protein, Gene Products, protein aggregate, Man, B61</description_synonyms><citation_count>0</citation_count><additional_accession>PXD003391</additional_accession></additional><is_claimable>true</is_claimable><name>LC-MS/MS analysis of B12 treated SH-SY5Y cells</name><description>B12 is a compound that has neuroprotective effects. We investigated the protein expression profile associated with the neuroprotective effects of B12 on human neuronal cells SH-SY5Y using label-free quantitative proteomics.</description><dates><publication>Tue Dec 29 22:41:00 GMT 2015</publication></dates><accession>MSV000079437</accession><cross_references><pubmed>26951766</pubmed></cross_references></HashMap>