Gene Report
Approved Symbol | IL1B |
---|---|
Approved Name | interleukin 1, beta |
Symbol Alias | IL1F2, IL-1B, IL1-BETA |
Location | 2q14 |
Position | chr2:113587337-113594356 (-) |
External Links |
Entrez Gene: 3553 Ensembl: ENSG00000125538 UCSC: uc002tii.1 HGNC ID: 5992 |
No. of Studies (Positive/Negative) | 3(2/1) |
Type | Literature-origin; SNP mapped; Protein mapped |
Name in Literature | Reference | Research Type | Statistical Result | Relation Description | |
---|---|---|---|---|---|
IL-1beta | Yu, 2003 | patients and normal controls | No significant difference was found in the genetic polymorph...... No significant difference was found in the genetic polymorphism between MDD patients and controls. However, MDD patients who were homozygous for the -511T allele of the IL-1beta gene had a trend of less severity of depressive symptoms and more favorable fluoxetine therapeutic response than -511C carriers. More... | ||
IL1B | Hwang, 2009 | patients and normal controls | P-value = 0.021 | Compared with depressed subjects carrying the -511C allele, ...... Compared with depressed subjects carrying the -511C allele, depressed subjects who were -511T homozygotes showed a significantly later depression age of onset of 7 years (P = 0.021). More... |
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Genetic/Epigenetic Locus | Protein and Other Molecule | Cell and Molecular Pathway | Neural System | Cognition and Behavior | Symptoms and Signs | Environment | MDD |
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Name in Literature | Reference | Research Type | Statistical Result | Relation Description |
---|---|---|---|---|
interleukin-1beta | Borkowska, 2011 | patients and normal controls | P-value=0.064 | A specific haplotype in this gene, composed of the C allele ...... A specific haplotype in this gene, composed of the C allele at -31 and the T allele at -511, has a tendency to have a statistically significant difference (p = 0.064) between patients and control group. More... |
#rs | Location | Annotation | No. of Studies (Positive/Negative) | |
---|---|---|---|---|
rs16944 | chr2:113594867(Forward) | upstream_gene_variant | 1(1/0) | |
rs1143643 | chr2:113588302(Forward) | downstream_gene_variant; intron_variant; nc_transcript_variant | 1(1/0) |
Approved Name | UniportKB | No. of Studies (Positive/Negative) | Source | |
---|---|---|---|---|
Interleukin-1 beta | P01584 | 6(4/2) | Literature-origin |
Literature-origin GO terms | ||||
ID | Name | Type | Evidence | |
---|---|---|---|---|
GO:0043491 | protein kinase B signaling cascade | biological process | IMP | |
GO:0006915 | apoptotic process | biological process | TAS[9218611] | |
GO:0000165 | MAPK cascade | biological process | IMP | |
GO:0006954 | inflammatory response | biological process | IDA[10748004]; NAS[1919436] |
Gene mapped GO terms | ||||
ID | Name | Type | Evidence | |
---|---|---|---|---|
GO:0030213 | hyaluronan biosynthetic process | biological process | IDA[15100360] | |
GO:0045080 | positive regulation of chemokine biosynthetic process | biological process | IEA | |
GO:0045893 | positive regulation of transcription, DNA-dependent | biological process | IDA[15100360] | |
GO:0007566 | embryo implantation | biological process | TAS[16720713] | |
GO:0051044 | positive regulation of membrane protein ectodomain proteolysis | biological process | IDA[18373975] | |
GO:0060355 | positive regulation of cell adhesion molecule production | biological process | NAS[19281832] | |
GO:0005829 | cytosol | cellular component | TAS | |
GO:0033198 | response to ATP | biological process | IEA | |
GO:0005125 | cytokine activity | molecular function | IDA[1919436]; IMP[2989698] | |
GO:0008285 | negative regulation of cell proliferation | biological process | IDA[3493774] | |
GO:0032308 | positive regulation of prostaglandin secretion | biological process | ISS | |
GO:0045086 | positive regulation of interleukin-2 biosynthetic process | biological process | IMP[2989698] | |
GO:0043407 | negative regulation of MAP kinase activity | biological process | ISS[16865359] | |
GO:0031622 | positive regulation of fever generation | biological process | ISS | |
GO:0070487 | monocyte aggregation | biological process | IDA[15100360] | |
GO:0070164 | negative regulation of adiponectin secretion | biological process | ISS[16865359] | |
GO:0045410 | positive regulation of interleukin-6 biosynthetic process | biological process | IEA | |
GO:0050996 | positive regulation of lipid catabolic process | biological process | ISS[16865359] | |
GO:0035066 | positive regulation of histone acetylation | biological process | NAS | |
GO:0060559 | positive regulation of calcidiol 1-monooxygenase activity | biological process | IDA[17023519] | |
GO:0051092 | positive regulation of NF-kappaB transcription factor activity | biological process | IDA[12958148] | |
GO:0043123 | positive regulation of I-kappaB kinase/NF-kappaB cascade | biological process | IEA | |
GO:0035690 | cellular response to drug | biological process | IDA[19158679] | |
GO:0001660 | fever generation | biological process | IEA | |
GO:0002711 | positive regulation of T cell mediated immunity | biological process | IC[1919436] | |
GO:0008083 | growth factor activity | molecular function | IEA | |
GO:0042346 | positive regulation of NF-kappaB import into nucleus | biological process | IDA[18390750] | |
GO:0043066 | negative regulation of apoptotic process | biological process | IDA[10748004] | |
GO:0030949 | positive regulation of vascular endothelial growth factor receptor signaling pathway | biological process | IC[12958148] | |
GO:0032757 | positive regulation of interleukin-8 production | biological process | IDA[19524870] | |
GO:0033129 | positive regulation of histone phosphorylation | biological process | NAS | |
GO:0045833 | negative regulation of lipid metabolic process | biological process | ISS[16865359] | |
GO:0005615 | extracellular space | cellular component | IDA[12483741]; IMP[3493774] | |
GO:0001934 | positive regulation of protein phosphorylation | biological process | IDA[10748004]; NAS[16477012] | |
GO:0006955 | immune response | biological process | IEA | |
GO:0010575 | positive regulation vascular endothelial growth factor production | biological process | IDA[12958148]; ISS | |
GO:0000187 | activation of MAPK activity | biological process | IDA[10748004] | |
GO:0032729 | positive regulation of interferon-gamma production | biological process | IDA | |
GO:0032755 | positive regulation of interleukin-6 production | biological process | TAS[16865359] | |
GO:0046627 | negative regulation of insulin receptor signaling pathway | biological process | ISS[16865359] | |
GO:0046827 | positive regulation of protein export from nucleus | biological process | NAS[19281832] | |
GO:0034116 | positive regulation of heterotypic cell-cell adhesion | biological process | IDA[15100360]; NAS[19281832] | |
GO:0071310 | cellular response to organic substance | biological process | IDA[19158679] | |
GO:0014805 | smooth muscle adaptation | biological process | NAS[16477012] | |
GO:0051091 | positive regulation of sequence-specific DNA binding transcription factor activity | biological process | IDA[10748004] | |
GO:0010829 | negative regulation of glucose transport | biological process | ISS[16865359] | |
GO:0045944 | positive regulation of transcription from RNA polymerase II promoter | biological process | IEA | |
GO:0071260 | cellular response to mechanical stimulus | biological process | IEP[19593445] | |
GO:0030730 | sequestering of triglyceride | biological process | IDA[19032770] | |
GO:0050796 | regulation of insulin secretion | biological process | IDA[8383325] | |
GO:0042102 | positive regulation of T cell proliferation | biological process | IDA[1919436] | |
GO:0043122 | regulation of I-kappaB kinase/NF-kappaB cascade | biological process | IDA[10748004] | |
GO:0045429 | positive regulation of nitric oxide biosynthetic process | biological process | IDA[8383325] | |
GO:0045840 | positive regulation of mitosis | biological process | IMP[2989698] | |
GO:0005149 | interleukin-1 receptor binding | molecular function | NAS[1919436] | |
GO:0071407 | cellular response to organic cyclic compound | biological process | IDA | |
GO:0030141 | secretory granule | cellular component | IEA | |
GO:0050995 | negative regulation of lipid catabolic process | biological process | IDA[19032770] | |
GO:0019904 | protein domain specific binding | molecular function | IPI[16575408] | |
GO:0032725 | positive regulation of granulocyte macrophage colony-stimulating factor production | biological process | IDA | |
GO:0007165 | signal transduction | biological process | TAS[9218611] | |
GO:0031663 | lipopolysaccharide-mediated signaling pathway | biological process | IDA | |
GO:0032611 | interleukin-1 beta production | biological process | IEA | |
GO:0030593 | neutrophil chemotaxis | biological process | IEA | |
GO:0019221 | cytokine-mediated signaling pathway | biological process | IDA[10748004] | |
GO:0046330 | positive regulation of JNK cascade | biological process | IEA | |
GO:0035505 | positive regulation of myosin light chain kinase activity | biological process | IDA[18390750] | |
GO:0051781 | positive regulation of cell division | biological process | IEA | |
GO:0007267 | cell-cell signaling | biological process | TAS[2989698] | |
GO:0045766 | positive regulation of angiogenesis | biological process | ISS | |
GO:0005576 | extracellular region | cellular component | IDA; NAS[1919436]; TAS | |
GO:0071639 | positive regulation of monocyte chemotactic protein-1 production | biological process | IDA[19524870] |
Literature-origin KEGG pathway | ||||
ID | Name | Brief Description | Full Description | |
---|---|---|---|---|
hsa04940 | type i_diabetes_mellitus | Type I diabetes mellitus | Type I diabetes mellitus is a disease that results from auto...... Type I diabetes mellitus is a disease that results from autoimmune destruction of the insulin-producing beta-cells. Certain beta-cell proteins act as autoantigens after being processed by antigen-presenting cell (APC), such as macrophages and dendritic cells, and presented in a complex with MHC-II molecules on the surface of the APC. Then immunogenic signals from APC activate CD4+ T cells, predominantly of the Th1 subset. Antigen-activated Th1 cells produce IL-2 and IFNgamma. They activate macrophages and cytotoxic CD8+ T cells, and these effector cells may kill islet beta-cells by one or both of two types of mechanisms: (1) direct interactions of antigen-specific cytotoxic T cells with a beta-cell autoantigen-MHC-I complex on the beta-cell, and (2) non-specific inflammatory mediators, such as free radicals/oxidants and cytokines (IL-1, TNFalpha, TNFbeta, IFNgamma). Type I diabetes is a polygenic disease. One of the principle determining genetic factors in diabetes incidence is the inheritance of mutant MHC-II alleles. Another plausible candidate gene is the insulin gene. More... | |
hsa05332 | graft versus_host_disease | Graft-versus-host disease | Graft-versus-host disease (GVHD) pathophysiology can be summ...... Graft-versus-host disease (GVHD) pathophysiology can be summerized in a three-step process. During step 1, the conditioning regimen (irradiation and/or chemotherapy) leads to damage, activation of host tissues and induction of inflammatory cytokines secretion. Increased expression of major histocompatibility complex (MHC) antigens and adhesion molecules leads to enhancement of the recognition of host MHC and/or minor histocompatibility antigens by mature donor T cells. Donor T-cell activation in step II is characterized by the predominance of Th1 cells and the secretion of IL-2 and IFN-gamma. These cytokines induce further T-cell expansion, induce cytotoxic T lymphocytes (CTL) and natural killer (NK) cells responses and prime additional mononuclear phagocytes to produce TNF-alpha and IL-1. Also, nitric oxide (NO) is produced by activated macrophages, and it may contribute to the tissue damage seen during step 3. Lipopolysaccharide (LPS), which leaks through the intestinal mucosa that was damaged during step 1, together with IFN-gamma, from step 2, further stimulate macrophages to secrete cytokines and NO. During step 3, the effector phase, activated CTL and NK cells mediate cytotoxicity against target host cells through Fas-Fas ligand interactions and perforin-granzyme B. More... |
Gene mapped KEGG pathways | ||||
ID | Name | Brief Description | Full Description | |
---|---|---|---|---|
hsa04060 | cytokine cytokine_receptor_interaction | Cytokine-cytokine receptor interaction | Cytokines are soluble extracellular proteins or glycoprotein...... Cytokines are soluble extracellular proteins or glycoproteins that are crucial intercellular regulators and mobilizers of cells engaged in innate as well as adaptive inflammatory host defenses, cell growth, differentiation, cell death, angiogenesis, and development and repair processes aimed at the restoration of homeostasis. Cytokines are released by various cells in the body, usually in response to an activating stimulus, and they induce responses through binding to specific receptors on the cell surface of target cells. Cytokines can be grouped by structure into different families and their receptors can likewise be grouped. More... | |
hsa05010 | alzheimers disease | Alzheimer's disease | Alzheimer's disease (AD) is a chronic disorder that slowly d...... Alzheimer's disease (AD) is a chronic disorder that slowly destroys neurons and causes serious cognitive disability. AD is associated with senile plaques and neurofibrillary tangles (NFTs). Amyloid-beta (Abeta), a major component of senile plaques, has various pathological effects on cell and organelle function. The extracellular Abeta oligomers may activate caspases through activation of cell surface death receptors. Alternatively, intracellular Abeta may contribute to pathology by facilitating tau hyper-phosphorylation, disrupting mitochondria function, and triggering calcium dysfunction. To date genetic studies have revealed four genes that may be linked to autosomal dominant or familial early onset AD (FAD). These four genes include: amyloid precursor protein (APP), presenilin 1 (PS1), presenilin 2 (PS2) and apolipoprotein E (ApoE). All mutations associated with APP and PS proteins can lead to an increase in the production of Abeta peptides, specifically the more amyloidogenic form, Abeta42. FAD-linked PS1 mutation downregulates the unfolded protein response and leads to vulnerability to ER stress. More... | |
hsa05020 | prion diseases | Prion diseases | Prion diseases, also termed transmissible spongiform encepha...... Prion diseases, also termed transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases that affect humans and a number of other animal species. The etiology of these diseases is thought to be associated with the conversion of a normal protein, PrPC, into an infectious, pathogenic form, PrPSc. The conversion is induced by prion infections (for example, variant Creutzfeldt-Jakob disease (vCJD), iatrogenic CJD, Kuru), mutations (familial CJD, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia (FFI)) or unknown factors (sporadic CJD (sCJD)), and is thought to occur after PrPC has reached the plasma membrane or is re-internalized for degradation. The PrPSc form shows greater protease resistance than PrPC and accumulates in affected individuals, often in the form of extracellular plaques. Pathways that may lead to neuronal death comprise oxidative stress, regulated activation of complement, ubiquitin-proteasome and endosomal-lysosomal systems, synaptic alterations and dendritic atrophy, corticosteroid response, and endoplasmic reticulum stress. In addition, the conformational transition could lead to the lost of a beneficial activity of the natively folded protein, PrPC. More... | |
hsa04620 | toll like_receptor_signaling_pathway | Toll-like receptor signaling pathway | Specific families of pattern recognition receptors are respo...... Specific families of pattern recognition receptors are responsible for detecting microbial pathogens and generating innate immune responses. Toll-like receptors (TLRs) are membrane-bound receptors identified as homologs of Toll in Drosophila. Mammalian TLRs are expressed on innate immune cells, such as macrophages and dendritic cells, and respond to the membrane components of Gram-positive or Gram-negative bacteria. Pathogen recognition by TLRs provokes rapid activation of innate immunity by inducing production of proinflammatory cytokines and upregulation of costimulatory molecules. TLR signaling pathways are separated into two groups: a MyD88-dependent pathway that leads to the production of proinflammatory cytokines with quick activation of NF-{kappa}B and MAPK, and a MyD88-independent pathway associated with the induction of IFN-beta and IFN-inducible genes, and maturation of dendritic cells with slow activation of NF-{kappa}B and MAPK. More... | |
hsa04621 | nod like_receptor_signaling_pathway | NOD-like receptor signaling pathway | Specific families of pattern recognition receptors are respo...... Specific families of pattern recognition receptors are responsible for detecting various pathogens and generating innate immune responses. The intracellular NOD-like receptor (NLR) family contains more than 20 members in mammals and plays a pivotal role in the recognition of intracellular ligands. NOD1 and NOD2, two prototypic NLRs, sense the cytosolic presence of the bacterial peptidoglycan fragments that escaped from endosomal compartments, driving the activation of NF-{kappa}B and MAPK, cytokine production and apoptosis. On the other hand, a different set of NLRs induces caspase-1 activation through the assembly of multiprotein complexes called inflammasomes. These NLRs include NALP1, NALP3 and Ipaf. The inflammasomes are critical for generating mature proinflammatory cytokines in concert with Toll-like receptor signaling pathway. More... | |
hsa04623 | cytosolic dna_sensing_pathway | Cytosolic DNA-sensing pathway | Specific families of pattern recognition receptors are respo...... Specific families of pattern recognition receptors are responsible for detecting foreign DNA from invading microbes or host cells and generating innate immune responses. DAI is the first identified sensor of cytosolic DNA which activates the IRF and NF-{kappa}B transcription factors, leading to production of type I interferon and other cytokines. The second type of cytoplasmic DNA sensor is AIM2. Upon sensing DNA, AIM2 triggers the assembly of the inflammasome, culminating in interleukin maturation. In addition to these receptors, there is a mechanism to sense foreign DNA, with the host RNA polymerase III converting the DNA into RNA for recognition by the RNA sensor RIG-I. These pathways provide various means to alert the cell. More... | |
hsa04210 | apoptosis | Apoptosis | Apoptosis is a genetically controlled mechanisms of cell dea...... Apoptosis is a genetically controlled mechanisms of cell death involved in the regulation of tissue homeostasis. The 2 major pathways of apoptosis are the extrinsic (Fas and other TNFR superfamily members and ligands) and the intrinsic (mitochondria-associated) pathways, both of which are found in the cytoplasm. The extrinsic pathway is triggered by death receptor engagement, which initiates a signaling cascade mediated by caspase-8 activation. Caspase-8 both feeds directly into caspase-3 activation and stimulates the release of cytochrome c by the mitochondria. Caspase-3 activation leads to the degradation of cellular proteins necessary to maintain cell survival and integrity. The intrinsic pathway occurs when various apoptotic stimuli trigger the release of cytochrome c from the mitochondria (independently of caspase-8 activation). Cytochrome c interacts with Apaf-1 and caspase-9 to promote the activation of caspase-3. Recent studies point to the ER as a third subcellular compartment implicated in apoptotic execution. Alterations in Ca2+ homeostasis and accumulation of misfolded proteins in the ER cause ER stress. Prolonged ER stress can result in the activation of BAD and/or caspase-12, and execute apoptosis. More... | |
hsa04640 | hematopoietic cell_lineage | Hematopoietic cell lineage | Blood-cell development progresses from a hematopoietic stem ...... Blood-cell development progresses from a hematopoietic stem cell (HSC), which can undergo either self-renewal or differentiation into a multilineage committed progenitor cell: a common lymphoid progenitor (CLP) or a common myeloid progenitor (CMP). A CLP gives rise to the lymphoid lineage of white blood cells or leukocytes-the natural killer (NK) cells and the T and B lymphocytes. A CMP gives rise to the myeloid lineage, which comprises the rest of the leukocytes, the erythrocytes (red blood cells), and the megakaryocytes that produce platelets important in blood clotting. Cells undergoing these differentiation process express a stage- and lineage-specific set of surface markers. Therefore cellular stages are identified by the specific expression patterns of these genes. More... | |
hsa05140 | leishmania infection | Leishmania infection | Leishmania is an intracellular protozoan parasite of macroph...... Leishmania is an intracellular protozoan parasite of macrophages that causes visceral, mucosal, and cutaneous diseases. The parasite is transmitted to humans by sandflies, where they survive and proliferate intracellularly by deactivating the macrophage. Successful infection of Leishmania is achieved by alteration of signaling events in the host cell, leading to enhanced production of the autoinhibitory molecules like TGF-beta and decreased induction of cytokines such as IL12 for protective immunity. Nitric oxide production is also inhibited. In addition, defective expression of major histocompatibility complex (MHC) genes silences subsequent T cell activation mediated by macrophages, resulting in abnormal immune responses. More... | |
hsa04010 | mapk signaling_pathway | MAPK signaling pathway | The mitogen-activated protein kinase (MAPK) cascade is a hig...... The mitogen-activated protein kinase (MAPK) cascade is a highly conserved module that is involved in various cellular functions, including cell proliferation, differentiation and migration. Mammals express at least four distinctly regulated groups of MAPKs, extracellular signal-related kinases (ERK)-1/2, Jun amino-terminal kinases (JNK1/2/3), p38 proteins (p38alpha/beta/gamma/delta) and ERK5, that are activated by specific MAPKKs: MEK1/2 for ERK1/2, MKK3/6 for the p38, MKK4/7 (JNKK1/2) for the JNKs, and MEK5 for ERK5. Each MAPKK, however, can be activated by more than one MAPKKK, increasing the complexity and diversity of MAPK signalling. Presumably each MAPKKK confers responsiveness to distinct stimuli. For example, activation of ERK1/2 by growth factors depends on the MAPKKK c-Raf, but other MAPKKKs may activate ERK1/2 in response to pro-inflammatory stimuli. More... |
Literature-origin BioCarta pathway | ||||
ID | Name | Brief Description | Full Description | |
---|---|---|---|---|
NTHI_PATHWAY | nthi pathway | NFkB activation by Nontypeable Hemophilus influenzae | The role of Hemophilus influenzae in ear infections and chro...... The role of Hemophilus influenzae in ear infections and chronic obstructive pulmonary disease includes the induction of an inflammatory response through activation of the transcription factor NF-kB. In addition to activation of inflammatory cytokine genes like IL-1 and TNF, H. influenzae activates TLR2 expression and genes involved in mucus production. Hemophilus influenzae activates NF-kB by multiple mechanisms, starting with activation of the Toll-like receptor 2 (TLR2) by the p16 protein in the H. influenzae outer membrane. TLR2 plays a key role in innate immune responses and is expressed in high levels in lymphoid cells as well as low levels in epithelial cells. The role of TLR2 was supported by blocking NF-kB activation with a dominant negative TLR2 and increasing it with transfection of a normal TLR2 gene. TLR2 in turn activates TAK1, which activates two divergent signaling pathways. One of these pathways leads to IkB kinase activation, IkB phosphorylation and degradation, releasing the NF-kB heterodimer to translocate into the nucleus and activate transcription of target genes. In the alternate pathway, TAK1 also activates NF-kB through a Map kinase pathway, activating p38 and NF-kB in a nuclear translocation independent manner. Investigation of the mechanisms of H. influenzae signaling involved in NF-kB activation may provide the information needed to develop better treatments for inflammatory conditions caused by this pathogen. Other pathways modulate the role of NF-kB in H. influenzae pathogenesis. Glucocorticoids widely used as anti-inflammatory drugs increase TLR2 activation by H. influenzae through the NIK/I-kB kinase pathway, while they repress the p38 dependent activation of NF-kB. The repression of the p38 pathway by glucocorticoids occurs through activation of the MAP kinase phosphatase-1 (MKP-1) which dephosphorylates and deactivates p38. Another aspect of the inflammatory response to H. influenzae infection is the production of excessive mucus, contributing to the overall symptoms of infection. NF-kB activation of the Muc2 gene contributes to mucus overproduction, in addition to H. influenzae activation of the TGF-beta receptor, activating SMAD transcription factors SMAD3 and SMAD4. Understanding mechanisms that modify H. influenzae signaling will contribute to further understanding the pathogenesis and treatment of ear infections and chronic obstructive pulmonary disease. More... |
Gene mapped BioCarta pathways | ||||
ID | Name | Brief Description | Full Description | |
---|---|---|---|---|
IL1R_PATHWAY | il1r pathway | Signal transduction through IL1R | Interleukin-1 (IL-1) is a pro-inflammatory cytokine that sig...... Interleukin-1 (IL-1) is a pro-inflammatory cytokine that signals primarily through the type 1 IL-1 receptor (IL-1R1). The activities of IL-1 include induction of fever, expression of vascular adhesion molecules, and roles in arthritis and septic shock. The inflammatory activities of IL-1 are partially derived by transcriptionally inducing expression of cytokines such as TNF-alpha and interferons, as well as inducing the expression of other inflammation-related genes. There are two forms of IL-1 encoded by distinct genes, IL-1 alpha and IL-1 beta. IL-1 beta is produced as a 269 amino acid precursor that is cleaved by IL-1beta converting enzyme (ICE) to the active IL-1 beta form that is secreted. IL-1 signaling is opposed by the naturally occurring peptide IL-1 receptor antagonist which is a therapeutic agent for the treatment of arthritis. The type 1 IL-1 receptor protein binds IL-1 beta but requires the IL-1 receptor accessory protein (IL-1RAcP) to transduce a signal. IL-1 binding causes activation of two kinases, IRAK-1 and IRAK-2, associated with the IL-1 receptor complex. IRAK-1 (IL-1 Receptor Associated Kinase) activates and recruits TRAF6 to the IL-1 receptor complex. TRAF6 activates two pathways, one leading to NF-kB activation and another leading to c-jun activation. The TRAF associated protein ECSIT leads to c-Jun activation through the Map kinase/JNK signaling system. TRAF6 also signals through the TAB1/TAK1 kinases to trigger the degradation of I-kB, and activation of NF-kB. The IL-1 signaling cascade represents a highly conserved response to pathogens through evolution, with homologs in insects and even in plants. The signal transduction cascade utilized by IL-1 receptor is similar to that of TNF, resulting in NF-kB activation, and is most similar to that of the Toll-like receptors that also participate in inflammatory signaling responses to pathogen components like endotoxin. More... | |
IL5_PATHWAY | il5 pathway | IL 5 Signaling Pathway | IL-5 is an inflammatory signaling molecule that primarily st...... IL-5 is an inflammatory signaling molecule that primarily stimulates eosinophil proliferation, maturation and activation. Eosinophils are leukocytes involved in inflammatory responses that defend against parasites and cause some aspects of asthma, allergic reactions, and perhaps autoimmune disorders. The action of IL-5 begins with an immune response in tissues, such as activation of macrophages and T cells that secrete IL-1, IL-4 and IL-6. The immune response can lead to IL-5 secretion by T cells, eosinophils and mast cells. Secreted IL-5 stimulates production and maturation of eosinophils in bone marrow that migrate to tissues in response to eotaxin and release factors that damage tissues, causing some of the undesirable consequences of inflammation. The receptor for IL-5 is a heterodimer of an alpha subunit that is required for IL-5 selective binding and a beta subunit that is also part of the IL-3 and GM-CSF receptors. Binding of IL-5 to the IL-5 receptor at the cell surface activates JAK/STAT signaling pathways that regulate transcription, proliferation, and differentiation. More... |
IL1B related interactors from protein-protein interaction data in HPRD (count: 10)
Gene | Interactor | Interactor in MK4MDD? | Experiment Type | PMID | |
---|---|---|---|---|---|
IL1B | IL1B | Yes | in vitro;in vivo | 2946959 | |
IL1B | IL1R1 | No | in vitro | 9062193 | |
IL1B | IL1R2 | No | in vitro | 7878046 | |
IL1B | IL1RAP | No | in vitro | 9820540 | |
IL1B | CASP4 | No | in vitro | 1919001 , 7797510 | |
IL1B | PRTN3 | No | in vivo | 10339575 | |
IL1B | A2M | No | in vitro;in vivo | 9714181 , 2466831 | |
IL1B | ADRB2 | Yes | in vitro | 11238007 | |
IL1B | MMP2 | No | in vitro | 8663297 | |
IL1B | CASP1 | No | in vitro;in vivo | 7797510 , 1919001 |