BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.pdfhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091-biopax3.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091-biopax2.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091_url.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091_urn.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.vcmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.scihttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.pnghttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.xpphttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000091?filename=BIOMD0000000091.mprimaryOK200Carole ProctorManually curatedCataractAlzheimer's DiseaseParkinson's DiseaseL2V1https://www.ebi.ac.uk/biomodels/BIOMD000000009115610770falseBioModelsSBMLModelsProctor2005 Actions of chaperones and their role in ageing2005MODEL2223638385Proctor CJ, Soti C, Boys RJ, Gillespie CS, Shanley DP, Wilkinson DJ, Kirkwood TBProctor CJ15610770,
Many molecular chaperones are also known as heat shock proteins because they are synthesised in increased amounts after brief exposure of cells to elevated temperatures. They have many cellular functions and are involved in the folding of nascent proteins, the re-folding of denatured proteins, the prevention of protein aggregation, and assisting the targeting of proteins for degradation by the proteasome and lysosomes. They also have a role in apoptosis and are involved in modulating signals for immune and inflammatory responses. Stress-induced transcription of heat shock proteins requires the activation of heat shock factor (HSF). Under normal conditions, HSF is bound to heat shock proteins resulting in feedback repression. During stress, cellular proteins undergo denaturation and sequester heat shock proteins bound to HSF, which is then able to become transcriptionally active. The induction of heat shock proteins is impaired with age and there is also a decline in chaperone function. Aberrant/damaged proteins accumulate with age and are implicated in several important age-related conditions (e.g. Alzheimer's disease, Parkinson's disease, and cataract). Therefore, the balance between damaged proteins and available free chaperones may be greatly disturbed during ageing. We have developed a mathematical model to describe the heat shock system. The aim of the model is two-fold: to explore the heat shock system and its implications in ageing; and to demonstrate how to build a model of a biological system using our simulation system (biology of ageing e-science integration and simulation (BASIS)).. null, 126.
Henry Wellcome Laboratory for Biogerontology Research, School of Clinical and Medical Sciences-Gerontology, University of Newcastle, Newcastle upon Tyne NE4 6BE, UK. c.j.proctor@ncl.ac.ukc.j.proctor@ncl.ac.ukUniversity of NewcastleBIOMD0000000091Many molecular chaperones are also known as heat shock proteins because they are synthesised in increased amounts after brief exposure of cells to elevated temperatures. They have many cellular functions and are involved in the folding of nascent proteins, the re-folding of denatured proteins, the prevention of protein aggregation, and assisting the targeting of proteins for degradation by the proteasome and lysosomes. They also have a role in apoptosis and are involved in modulating signals for immune and inflammatory responses. Stress-induced transcription of heat shock proteins requires the activation of heat shock factor (HSF). Under normal conditions, HSF is bound to heat shock proteins resulting in feedback repression. During stress, cellular proteins undergo denaturation and sequester heat shock proteins bound to HSF, which is then able to become transcriptionally active. The induction of heat shock proteins is impaired with age and there is also a decline in chaperone function. Aberrant/damaged proteins accumulate with age and are implicated in several important age-related conditions (e.g. Alzheimer's disease, Parkinson's disease, and cataract). Therefore, the balance between damaged proteins and available free chaperones may be greatly disturbed during ageing. We have developed a mathematical model to describe the heat shock system. The aim of the model is two-fold: to explore the heat shock system and its implications in ageing; and to demonstrate how to build a model of a biological system using our simulation system (biology of ageing e-science integration and simulation (BASIS)).Modelling the actions of chaperones and their role in ageing.Proctor Carole J CJ, Soti Csaba C, Boys Richard J RJ, Gillespie Colin S CS, Shanley Daryl P DP, Wilkinson Darren J DJ, Kirkwood Thomas B L TBConcept, Role, Concepts, Role Concept, Roles, ageing., Role Conceptsmulticellular organismal catabolic process, single-organism catabolic process, Presenile Alzheimer Dementia, Parkinson's disease, Opacities, ALZHEIMERS DIS, heat-shock protein, HSN1E, Early Onset, Parkinson's disease NOS, Ass-1, opacity of the lens, protein, Sciences., Autolysosome, type I programmed cell death, Alzheimer's disease, Circulatory Collapse, dysfunctional, AD, protein polypeptide chains, unspecified, Chaperone, Extrinsic Pathway Apoptoses, dHSFa, Roles, Programmed, Hot, AA408052, IL-6, Concepts, fold, Heat, protein aggregate, Shock, D-HSF, average, increased, LATE ONSET ALZHEIMER DIS, Parkinson disease, DAT - Dementia Alzheimer's type, Parkinson's disease (disorder), Molecular, catabolism, activation inducer molecule, proteins, elevated, Opacity, free, ASS, Cataract, DNA-dependent, Intrinsic Pathway Apoptosis, cataract, l(2)03091, AD - Alzheimer's disease, Classic, Alzheimer Type Dementia, Role Concepts, Classical Apoptosis, 26S proteasome, ALZHEIMER DIS EARLY ONSET, Parkinson syndrome, Presenile, Membranous, transcription from bacterial-type RNA polymerase promoter, Alzheimers disease, Parkinson's syndrome, cellular suicide, Senile, Parkinsons, Caspase-Dependent Apoptosis, DNA-dependent transcription, aberrant, Acute Confusional Senile Dementia, Heat Shock Protein, Circulatory Failure, Normalcy, HSF, Hsf, Autolysosomes, Alzheimer's Dementia, partial functionality, Alzheimer Type, DmHSF, BSF2, HSP, Role Concept, signaling (initiator) caspase activity, induction of apoptosis, Intrinsic Pathway, Extrinsic Pathway Apoptosis, Role, NOS, Individual, Caspase-Dependent, hsf, activation, Dementia, proteasome, early T-cell activation antigen p60, ADCADN, Alzheimers, breakdown, Alzheimer, Lens Opacities, Dementias, Cell Death, HSF1, lacks function of type, low functionality, Intrinsic Pathway Apoptoses, organ system, IFNB2, Health, induction of apoptosis by p53, Senile Dementia, paralysis agitans, bacterial transcription, Extrinsic Pathway, Hot Temperatures, Alzheimer's Disease, Feedbacks, Classical, Apoptoses, CD69, accessory, Dementia of the Alzheimer's type, atypia, transcription, Lysosome, HSFa, Circulatory, caspase-dependent programmed cell death, Gene, Caspase Dependent Apoptosis, impaired, EA1, MLR-3, protein-containing complex, apoptotic programmed cell death, Focal Onset, Normalcies, supernumerary, body system, activation of apoptosis, Failure, unspecified (disorder), ALZHEIMER DIS, AIM, HGF, polypeptide chain, [X]Dementia in Alzheimer's disease, Gene Products, system, atypical, Membranous Cataract, Type I, early activation antigen CD69, Lens, Normalities, Heat Shock Proteins, anatomical systems, dysfunction, apoptosis activator activity, CG5748, Idiopathic PD, FOCAL ONSET ALZHEIMERS DIS, Hypovolemic Shock, Membranous Cataracts, Hypovolemic, DmHSFa, leukocyte surface antigen Leu-23, Pseudoaphakias, Dm-Hsf, Classic Apoptosis, Alzheimer Disease, execution phase of apoptotic process, C-type lectin domain family 2 member C, Alzheimer's disease (disorder), programmed cell death by apoptosis, Alzheimers Dementia, high elevation, Apoptosis, Cataracts, Alzheimer Senile Dementia, xhsf1, Individual Health, cellular transcription, Disease, cell suicide, degradation, Chaperones, protein complex, Proteins, apoptotic cell death, DNMT, function, defective, Pseudoaphakia, Molecular Chaperone, dHSF, MCMT, Cell, Primary Senile Degenerative Dementia, Concept, [X]Dementia in Alzheimer's disease (disorder), BL-AC/P26, Temperatures, native protein, natural protein, Programmed Cell Death, Protein, connected anatomical system, CXXC9, apoptosis signaling, Temperature, apoptosis, Normality, Dementia in Alzheimer's disease, increased number, DNA-templated, Alzheimer's Disease Pathway, stress protein, Alzheimer Dementia, cataract (disease), Protein Gene Products, Classic Apoptoses, Collapse, Parkinsonian disorder, present in greater numbers in organism, Gene Proteins, ageing, having decreased function, Late Onset, DmelCG5748, Parkinson's disease NOS (disorder), GP32/28, apoptotic program, Dementia in Alzheimer's disease (disorder), commitment to apoptosis, Lens Opacity, CLEC2Cextent, multicellular organismal catabolic process, single-organism catabolic process, Presenile Alzheimer Dementia, Parkinson's disease, Opacities, ALZHEIMERS DIS, Public Sectors, heat-shock protein, HSN1E, Early Onset, Parkinson's disease NOS, Ass-1, opacity of the lens, protein, Autolysosome, type I programmed cell death, Alzheimer's disease, Circulatory Collapse, dysfunctional, AD, protein polypeptide chains, unspecified, Chaperone, Extrinsic Pathway Apoptoses, dHSFa, Roles, Programmed, Hot, AA408052, IL-6, Concepts, fold, Heat, Public Enterprise, protein aggregate, Shock, D-HSF, average, increased, LATE ONSET ALZHEIMER DIS, Parkinson disease, DAT - Dementia Alzheimer's type, Parkinson's disease (disorder), Molecular, catabolism, activation inducer molecule, Public Domains, proteins, elevated, Boys, Opacity, free, ASS, Cataract, DNA-dependent, Intrinsic Pathway Apoptosis, cataract, l(2)03091, AD - Alzheimer's disease, Classic, Alzheimer Type Dementia, Role Concepts, Classical Apoptosis, 26S proteasome, ALZHEIMER DIS EARLY ONSET, Parkinson syndrome, Presenile, Membranous, transcription from bacterial-type RNA polymerase promoter, Alzheimers disease, Parkinson's syndrome, cellular suicide, Senile, Parkinsons, Caspase-Dependent Apoptosis, DNA-dependent transcription, aberrant, completeness, Acute Confusional Senile Dementia, Heat Shock Protein, Circulatory Failure, Normalcy, HSF, Hsf, Autolysosomes, Alzheimer's Dementia, partial functionality, Alzheimer Type, DmHSF, BSF2, HSP, Role Concept, signaling (initiator) caspase activity, induction of apoptosis, Intrinsic Pathway, Public Domain, Extrinsic Pathway Apoptosis, Role, Domains, NOS, Individual, Caspase-Dependent, hsf, activation, Domain, Dementia, proteasome, early T-cell activation antigen p60, ADCADN, Alzheimers, breakdown, Alzheimer, Lens Opacities, Dementias, Cell Death, HSF1, lacks function of type, low functionality, Intrinsic Pathway Apoptoses, organ system, IFNB2, Health, Sector, induction of apoptosis by p53, Senile Dementia, paralysis agitans, bacterial transcription, Extrinsic Pathway, Hot Temperatures, Alzheimer's Disease, Feedbacks, Classical, Apoptoses, CD69, accessory, Dementia of the Alzheimer's type, atypia, transcription, Sectors, Lysosome, HSFa, Circulatory, caspase-dependent programmed cell death, number, Gene, Caspase Dependent Apoptosis, impaired, EA1, Copyrights, MLR-3, protein-containing complex, apoptotic programmed cell death, Focal Onset, Normalcies, supernumerary, body system, presence, activation of apoptosis, Failure, unspecified (disorder), ALZHEIMER DIS, AIM, HGF, polypeptide chain, [X]Dementia in Alzheimer's disease, Gene Products, system, atypical, Membranous Cataract, Type I, early activation antigen CD69, Lens, Enterprises, Normalities, Heat Shock Proteins, anatomical systems, dysfunction, Sciences, apoptosis activator activity, Public Enterprises, CG5748, Idiopathic PD, FOCAL ONSET ALZHEIMERS DIS, Hypovolemic Shock, Membranous Cataracts, Hypovolemic, DmHSFa, leukocyte surface antigen Leu-23, Abstract, Pseudoaphakias, Dm-Hsf, Classic Apoptosis, Alzheimer Disease, execution phase of apoptotic process, C-type lectin domain family 2 member C, Alzheimer's disease (disorder), Enterprise, programmed cell death by apoptosis, Alzheimers Dementia, high elevation, Apoptosis, Cataracts, Alzheimer Senile Dementia, xhsf1, Individual Health, cellular transcription, Disease, cell suicide, degradation, Chaperones, protein complex, Proteins, apoptotic cell death, DNMT, function, defective, Pseudoaphakia, Molecular Chaperone, dHSF, MCMT, Cell, Primary Senile Degenerative Dementia, Concept, [X]Dementia in Alzheimer's disease (disorder), BL-AC/P26, count in organism, Temperatures, native protein, natural protein, Public, Programmed Cell Death, Protein, connected anatomical system, Data Base, CXXC9, apoptosis signaling, Temperature, apoptosis, Normality, Dementia in Alzheimer's disease, increased number, DNA-templated, Alzheimer's Disease Pathway, stress protein, Alzheimer Dementia, cataract (disease), Collapse, Protein Gene Products, Classic Apoptoses, Parkinsonian disorder, ageing, Gene Proteins, present in greater numbers in organism, having decreased function, Late Onset, DmelCG5748, Parkinson's disease NOS (disorder), GP32/28, apoptotic program, Dementia in Alzheimer's disease (disorder), commitment to apoptosis, Lens Opacity, Public., quantitative, CLEC2C, presence or absence in organismConcept, Role, Concepts, Role Concept, Roles, ageing., Role ConceptsfalseProctor2005 - Actions of chaperones and their role in ageing
Proctor2005 - Actions of chaperones and their
role in ageing
This model is described in the article:
Modelling the actions of
chaperones and their role in ageing.
Proctor CJ, Soti C, Boys RJ,
Gillespie CS, Shanley DP, Wilkinson DJ, Kirkwood TB.
Mech. Ageing Dev. 2005 Jan; 126(1):
119-131
Abstract:
Many molecular chaperones are also known as heat shock
proteins because they are synthesised in increased amounts
after brief exposure of cells to elevated temperatures. They
have many cellular functions and are involved in the folding of
nascent proteins, the re-folding of denatured proteins, the
prevention of protein aggregation, and assisting the targeting
of proteins for degradation by the proteasome and lysosomes.
They also have a role in apoptosis and are involved in
modulating signals for immune and inflammatory responses.
Stress-induced transcription of heat shock proteins requires
the activation of heat shock factor (HSF). Under normal
conditions, HSF is bound to heat shock proteins resulting in
feedback repression. During stress, cellular proteins undergo
denaturation and sequester heat shock proteins bound to HSF,
which is then able to become transcriptionally active. The
induction of heat shock proteins is impaired with age and there
is also a decline in chaperone function. Aberrant/damaged
proteins accumulate with age and are implicated in several
important age-related conditions (e.g. Alzheimer's disease,
Parkinson's disease, and cataract). Therefore, the balance
between damaged proteins and available free chaperones may be
greatly disturbed during ageing. We have developed a
mathematical model to describe the heat shock system. The aim
of the model is two-fold: to explore the heat shock system and
its implications in ageing; and to demonstrate how to build a
model of a biological system using our simulation system
(biology of ageing e-science integration and simulation
(BASIS)).
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BIOMD0000000091.
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2014-06-032007-02-262007-03-08BIOMD000000009115610770CHEBI:26523CHEBI:15422CHEBI:16761MODEL2223638385BIOMD0000000091GO:0051085GO:0007569GO:0009408GO:0005623GO:0043234GO:0009059GO:0022417GO:0051879GO:0043624GO:0042026GO:0016887GO:0043623GO:0006351GO:0044257GO:0006757GO:0006800GO:0016209C00002C00008131567IPR001404IPR000232