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- Data Summary
Gene Report
Approved Symbol | BDKRB2 |
---|---|
Symbol Alias | BK-2 |
Approved Name | bradykinin receptor B2 |
Location | 14q32.1-q32.2 |
Position | chr14:96671135-96710666, + |
External Links |
HGNC: 1030 Entrez Gene: 624 Ensembl: ENSG00000168398 UCSC: uc010avm.1 |
No. of Studies | 0 (significant: 0; non-significant: 0; trend: 0) |
Source | Mapped by PBA pathway |
GO terms by PBA (with statistical significance of FDR<0.05) (count: 1)
ID | Name | Type | Evidence[PMID] | No. of Genes in ADHDgene |
---|---|---|---|---|
GO:0016298 | lipase activity | Molecular Function | 49 |
GO terms by database search (count: 22)
ID | Name | No. of Genes in ADHDgene | Brief Description |
---|---|---|---|
hsa04080 | Neuroactive ligand-receptor interaction | 93 | |
hsa04020 | Calcium signaling pathway | 63 | Ca2+ that enters the cell from the outside is a principal so...... Ca2+ that enters the cell from the outside is a principal source of signal Ca2+. Entry of Ca2+ is driven by the presence of a large electrochemical gradient across the plasma membrane. Cells use this external source of signal Ca2+ by activating various entry channels with widely different properties. The voltage-operated channels (VOCs) are found in excitable cells and generate the rapid Ca2+ fluxes that control fast cellular processes. There are many other Ca2+-entry channels, such as the receptor-operated channels (ROCs), for example the NMDA (N-methyl-D-aspartate) receptors (NMDARs) that respond to glutamate. There also are second-messenger-operated channels (SMOCs) and store-operated channels (SOCs). More... |
hsa04810 | Regulation of actin cytoskeleton | 48 | |
hsa05142 | Chagas disease (American trypanosomiasis) | 23 | Trypanosoma cruzi is an intracellular protozoan parasite tha...... Trypanosoma cruzi is an intracellular protozoan parasite that causes Chagas disease. The parasite life cycle involves hematophagous reduviid bugs as vectors. Once parasites enter the host body, they invade diverse host cells including cardiomyocytes. Establishment of infection depends on various parasite molecules such as cruzipain, oligopeptidase B, and trans-sialidase that activate Ca2+ signaling. Internalized parasites escape from the parasitophorous vacuole using secreted pore-forming TcTOX molecule and replicate in the cytosol. Multiplied parasites eventually lyse infected host cells and are released in the circulation. During these events, the parasites manipulate host innate immunity and elicit cardiomyocyte hypertrophy. T lymphocyte responses are also disturbed. More... |
hsa04961 | Endocrine and other factor-regulated calcium reabsorption | 8 | Calcium (Ca2+) is essential for numerous physiological funct...... Calcium (Ca2+) is essential for numerous physiological functions including intracellular signalling processes, neuronal excitability, muscle contraction and bone formation. Therefore, its homeostasis is finely maintained through the coordination of intestinal absorption, renal reabsorption, and bone resorption. In kidney, the late part of the distal convoluted tubule (DCT) and the connecting tubule (CNT) are the site of active Ca2+ transport and precisely regulate Ca2+ reabsorption. Following Ca2+ entry through TRPV5, Ca2+ bound to calbindin-D28K diffuses to the basolateral side, where it is extruded into the blood compartment through NCX1 and to a lesser extent PMCA1b. In the urinary compartment, both klotho and tissue kallikrein (TK) increase the apical abundance of TRPV5. In the blood compartment, PTH, 1,25(OH)2D3 and estrogen increase the transcription and protein expression of the luminal Ca2+ channels, calbindins, and the extrusion systems. More... |
hsa04610 | Complement and coagulation cascades | 12 | The complement system is a proteolytic cascade in blood plas...... The complement system is a proteolytic cascade in blood plasma and a mediator of innate immunity, a nonspecific defense mechanism against pathogens. There are three pathways of complement activation: the classical pathway, the lectin pathway, and the alternative pathway. All of these pathways generate a crucial enzymatic activity that, in turn, generates the effector molecules of complement. The main consequences of complement activation are the opsonization of pathogens, the recruitment of inflammatory and immunocompetent cells, and the direct killing of pathogens. Blood coagulation is another series of proenzyme-to-serine protease conversions, culminating the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. Protease-activated receptors, such as those activated by thrombin, are members of G protein-coupled receptors and function as a mediator of innate immunity. The kallikrein-kinin system is an endogenous metabolic cascade, triggering of which results in the release of vasoactive kinins (bradykinin-related peptides). Kinin peptides are implicated in many physiological and pathological processes including the regulation of blood pressure and sodium homeostasis, inflammatory processes, and the cardioprotective effects of preconditioning. More... |
Region: chr14:96671135..96710666 View in gBrowse
Copyright: Bioinformatics Lab, Institute of Psychology, Chinese Academy of Sciences Feedback
Last update: Feb 26, 2014