Showing posts with label Kegg. Show all posts
Showing posts with label Kegg. Show all posts
KEGG pathway analysis of the genes implicated in chronic fatigue syndrome
There are relatively few genetic studies on chronic fatigue syndrome /fibromyalgia compared to other disorders, and a systems biology approach is necessarily limited. The main thrust so far seems to be related to neurotransmitter systems,(dopamine/ glutamate and serotonin) but also to the immune network and viral and pathogen related pathways.
Alzheimer's Pathways: An update of KEGG pathways (BIN1, CD33, CD2AP. MS4A2, etc)
These pathways include novel genes and a number of new pathways recently added by KEGG: Compounds relevant to Alzheimer's disease (cholesterol, homocysteine, vitamins, etc.) have been added, and proteins related to the herpes simplex life cycle are also colour-coded.
Alzheimer's genes and risk factors :
Alzheimer's genes and risk factors :
KEGG pathway analysis of the AIDS virus HIV1/host interactome
Image via WikipediaOther KEGG pathways
Huntington's disease: KEGG pathway analysis of the Huntingtin interactome
KEGG pathway analysis of the HTT huntingtin interactome in Huntington's disease
Other KEGG posts
Other KEGG pathways
Other KEGG posts
Other KEGG pathways
KEGG pathway analysis of Autism susceptibility genes
This analysis of several hundred Autism susceptibility gene candidates highlights MAPK, calcium, and neurotrophin pathways, among others, as well as numerous adhesion related networks. As with many other diseases, immune networks are well represented , as are pathogen entry and defence pathways.
Other KEGG pathway analyses of polygenic diseases
Other KEGG pathway analyses of polygenic diseases
KEGG pathway analysis of the AIDS virus HIV-1/host interactome
The HIV-1 AIDS virus interacts with a large number of host proteins which etch out a number of signalling networks. These are related to the viral life cycle and to pathogen defense and to many immune related pathways. Pathways related to comorbid conditions such as NeuroAids, dementia or psychosis are also well represented.
Herpes simplex host/pathogen interactome
Herpes simplex host/pathogen interactome
KEGG pathway analysis of over 400 Bipolar disorder susceptibility genes
These pathways, etched out by hundreds of genes, pre and post GWAS, include many brain related pathways, but also many related to the immune system and pathogen entry pathways. Pathogen risk factors are referenced here Bipolar disorder risk factors This trilogy appears to be a common theme in these polygenic diseases and the genes are implicated in brain and neurotransmitter pathology but also in the the life cycles of the pathogens implicated as risk factors.
Other Kegg pathways Alzheimer's Parkinson's Schizophrenia Herpes simplex infection Cystic fibrosis CFTR interactome
Other Kegg pathways Alzheimer's Parkinson's Schizophrenia Herpes simplex infection Cystic fibrosis CFTR interactome
Kegg pathway analysis of over 400 Alzheimer's disease susceptibility genes
Over 400 Alzheimer’s disease susceptibility genes have been recorded in association studies.This Kegg pathway analysis shows that these genes trace out a number of signalling networks that are highly relevant to the sub-pathologies of Alzheimer’s disease. These genes are colour-coded yellow while genes also involved in the herpes simplex life cycle are coded red.
These pathways include the APP processing pathway as well as apoptosis and oxidative stress related networks. Pathways involved in glycolysis, the Krebs cycle and oxidative phosphorylation are also implicated, a testament to the problems in cerebral energy metabolism, observed in Alzheimer’s disease.
Numerous immune and pathogen defence pathways are involved, as are a number of clearly defined pathogen entry pathways. Some of the more exotic pathways, for example Chaga’s disease and amoebiasis should perhaps be considered as generic rather than specific, indicating general routes for pathogen entry. These pathways tie in with the diverse viral, bacterial and other pathogens that have been implicated as Alzheimer’s disease risk factors( e.g. Chlamydia , C.Neoformans, herpes simplex or helicobacter pylori) See database
Despite the problems of replication, these genes, collected over decades of genetic association studies, tell a story that illustrates the aetiology of Alzheimer’s disease. The pathways etched out by these genes are relevant to many of the processes known to be disrupted in this disorder, and also to the pathogenic environmental risk factors.
Other Kegg pathways
These pathways include the APP processing pathway as well as apoptosis and oxidative stress related networks. Pathways involved in glycolysis, the Krebs cycle and oxidative phosphorylation are also implicated, a testament to the problems in cerebral energy metabolism, observed in Alzheimer’s disease.
Numerous immune and pathogen defence pathways are involved, as are a number of clearly defined pathogen entry pathways. Some of the more exotic pathways, for example Chaga’s disease and amoebiasis should perhaps be considered as generic rather than specific, indicating general routes for pathogen entry. These pathways tie in with the diverse viral, bacterial and other pathogens that have been implicated as Alzheimer’s disease risk factors( e.g. Chlamydia , C.Neoformans, herpes simplex or helicobacter pylori) See database
Despite the problems of replication, these genes, collected over decades of genetic association studies, tell a story that illustrates the aetiology of Alzheimer’s disease. The pathways etched out by these genes are relevant to many of the processes known to be disrupted in this disorder, and also to the pathogenic environmental risk factors.
Other Kegg pathways
Bioinformatics analysis of homologies between pathogen antigens, autoantigens and the CFTR cystic fibrosis protein: A role for immunoadsorption therapy? : Nature Precedings
There has been quite a lot of interest in the cystic fibrosis KEGG pathway analysis of the CFTR interactome, so I have posted this at NaturePrecedings under a creative commons license.
The cystic fibrosis CFTR chloride channel is involved in pathogen entry into epithelial cells, and provides the glutathione and hypochlorous acid necessary for bactericidal and viricidal actions. CFTR mutations block these effects, diminishing pathogen defence and allowing pathogen accumulation in the extracellular space, where antibody encounter is likely. The pathogen antigens observed in cystic fibrosis (including P.Aeruginosa, S.Aureus and S.Maltophilia proteins) are homologous to the autoantigens reported in cystic fibrosis and all are homologous to the CFTR protein itself. Antibodies to pathogens and autoantigens may also target the CFTR protein, acting as antagonists, further compromising its function. The tripartite relationship between pathogen antigens, autoantigens and the CFTR protein creates a feed forward cycle, diminishing the function of the CFTR protein and increasing the probability of pathogen accumulation and further antibody encounters at every turn. Kegg pathway analysis of the CFTR/autoantigen interactome indicates that the CFTR protein is also involved in pathogen entry pathways, diabetes and pancreatic and gastric acid secretion pathways, in pathways related to cardiac myopathy, and in the gonadotrophin signalling network, all which are relevant to cystic fibrosis. Interruption of this cycle by antigen and antibody adsorption, and possibly by immunosuppressant therapy may perhaps be of clinical benefit in cystic fibrosis.
The cystic fibrosis CFTR chloride channel is involved in pathogen entry into epithelial cells, and provides the glutathione and hypochlorous acid necessary for bactericidal and viricidal actions. CFTR mutations block these effects, diminishing pathogen defence and allowing pathogen accumulation in the extracellular space, where antibody encounter is likely. The pathogen antigens observed in cystic fibrosis (including P.Aeruginosa, S.Aureus and S.Maltophilia proteins) are homologous to the autoantigens reported in cystic fibrosis and all are homologous to the CFTR protein itself. Antibodies to pathogens and autoantigens may also target the CFTR protein, acting as antagonists, further compromising its function. The tripartite relationship between pathogen antigens, autoantigens and the CFTR protein creates a feed forward cycle, diminishing the function of the CFTR protein and increasing the probability of pathogen accumulation and further antibody encounters at every turn. Kegg pathway analysis of the CFTR/autoantigen interactome indicates that the CFTR protein is also involved in pathogen entry pathways, diabetes and pancreatic and gastric acid secretion pathways, in pathways related to cardiac myopathy, and in the gonadotrophin signalling network, all which are relevant to cystic fibrosis. Interruption of this cycle by antigen and antibody adsorption, and possibly by immunosuppressant therapy may perhaps be of clinical benefit in cystic fibrosis.
Kegg pathways traced out by schizophrenia susceptibility genes
Over 600 genes have been implicated in schizophrenia, and GWAS studies have continued to subscribe to the idea of multiple genes of small effect. Kegg pathway analysis of these genes highlights some well known pathways that have already been described , including long term potentiation and oxidative stress refs dopamine pathways refs neuregulin and growth pathways refs and adhesion pathways refs among others, as might be expected in the context of schizophrenia pathology. A large number of immune-related pathways are covered by the these genes again in agreement with prior data refs. In addition, several pathogen entry pathways are highly represented with toxoplasmosis refs heading the list. Viral entry pathways are also prominent refs , supporting the idea that genes and pathogens are interdependent refs. Many pathways thus contribute to different endophenotypes and pathological processes in schizophrenia.
Other pathways
Other pathways
KEGG pathway analysis of the Herpes simplex host/pathogen interactome
During its life cycle the herpes simplex virus interacts with a number of host proteins (see database ). KEGG pathway analysis of these proteins illustrates the cellular processes usurped by the virus: for example adhesion molecules that are used for entry, endocytosis pathways, the actin skeleton or protein processing, and shows where the virus interferes with key immune related processes, for example antigen processing. The use of these proteins by the virus interferes with their normal function. Interestingly, a number of these pathways are related to human disease, including Alzheimer's disease. HSV-1 infection has been reported as a risk factor in Alzheimer's disease, and a number of key Alzheimer's disease gene products are also involved in the viral life cycle (see database) The proteins used by the virus are also implicated in a number of pathogen entry pathways, for example Toxoplasmosis or Helicobacter Pylori infection, suggesting that one infection may influence another. These types of interactomes are useful for determining sites of viral interference from the host's perspective.
Other pathways
Other pathways
Parkinson's disease signalling pathways traced out by susceptibility genes
As with many other polygenic diseases, the genes implicated in Parkinson's disease trace out sets of pathways that relate to each other, and to the risk factors implicated in the disease. A Kegg pathway analysis of the genes implicated in Parkinson's disease is shown on this post. Mitochondrial and oxidative phosphorylation genes can evidently be related to the mitochondrial toxins, MPTP , rotenone and paraquat , and cytochrome p450 and xenobiotic metabolism genes can also be related to environmental toxins. Generic pathogen entry pathways relate to viruses and pathogens that have been implicated as risk factors (influenza, coronavirus Herpes simplex. T.Gondii and Helicobacter pylori). Chemokine, cytokine and T-cell pathways related to the immune system could also be considered in terms of pathogen defence, as can Toll receptor, NOD and RIG pathways. (see risk factor database)
Living in a rural environment and the use of pesticides have been implicated as environmental risk factors.
Clearly, not everyone in this situation develops Parkinson's disease, but they may do so if the p450 and other metabolism related genes are less able to deal with these toxins, or if the mitochondrial genes render the mitochondrial proteins more sensitive to their effects.
Genes and risk factors likely work together via these and other pathways. GWAS will no doubt unearth more genes, but those already existing, together with the environmental risk factors tell a story that is highly relevant to our understanding of Parkinson's disease. GWAS studies, because of the large numbers used, may iron out these environmental interactions, but partitioning the data in relation to environmental effects may be informative.
These maps are from the Kegg pathway database , under the conditions of an academic licence, with thanks.
Other pathways
Living in a rural environment and the use of pesticides have been implicated as environmental risk factors.
Clearly, not everyone in this situation develops Parkinson's disease, but they may do so if the p450 and other metabolism related genes are less able to deal with these toxins, or if the mitochondrial genes render the mitochondrial proteins more sensitive to their effects.
Genes and risk factors likely work together via these and other pathways. GWAS will no doubt unearth more genes, but those already existing, together with the environmental risk factors tell a story that is highly relevant to our understanding of Parkinson's disease. GWAS studies, because of the large numbers used, may iron out these environmental interactions, but partitioning the data in relation to environmental effects may be informative.
These maps are from the Kegg pathway database , under the conditions of an academic licence, with thanks.
Other pathways
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