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Monoclonal Antibody Immunoprecipitation Positive Regulation of Action Potential

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Voltage gated sodium channels are composed of a large alpha subunit and auxiliary beta subunits. The alpha subunit has 4 homologous domains, with each domain containing 6 transmembrane segments. These segments function as the voltage sensor and sodium permeable pore. Upon change of membrane potential, the sodium channel is activated, which allows sodium ions to flow through (1,2). When associated with beta subunits or other accessory proteins, the alpha subunit is regulated at the level of cell surface expression, kinetics, and voltage dependence (3,4).There are 9 mammalian alpha subunits, named Nav1.1-Nav1.9 (5). These alpha subunits differ in tissue specificity and biophysical functions (6,7). Seven of these subunits are essential for the initiation and propagation of action potentials in the central and peripheral nervous system while Nav1.4 and Nav1.5 are mainly expressed in skeletal muscle and cardiac muscle (8,9). Mutations in these alpha channel subunits have been identified in patients with epilepsy, seizure, ataxia, sensitivity to pain, and cardiomyopathy (reviewed in 10).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Voltage gated sodium channels are composed of a large alpha subunit and auxiliary beta subunits. The alpha subunit has 4 homologous domains, with each domain containing 6 transmembrane segments. These segments function as the voltage sensor and sodium permeable pore. Upon change of membrane potential, the sodium channel is activated, which allows sodium ions to flow through (1,2). When associated with beta subunits or other accessory proteins, the alpha subunit is regulated at the level of cell surface expression, kinetics, and voltage dependence (3,4).There are 9 mammalian alpha subunits, named Nav1.1-Nav1.9 (5). These alpha subunits differ in tissue specificity and biophysical functions (6,7). Seven of these subunits are essential for the initiation and propagation of action potentials in the central and peripheral nervous system while Nav1.4 and Nav1.5 are mainly expressed in skeletal muscle and cardiac muscle (8,9). Mutations in these alpha channel subunits have been identified in patients with epilepsy, seizure, ataxia, sensitivity to pain, and cardiomyopathy (reviewed in 10).

$122
20 µl
$293
100 µl
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: TNF-α, the prototypical member of the TNF protein superfamily, is a homotrimeric type-II membrane protein (1,2). Membrane-bound TNF-α is cleaved by the metalloprotease TACE/ADAM17 to generate a soluble homotrimer (2). Both membrane and soluble forms of TNF-α are biologically active. TNF-α is produced by a variety of immune cells including T cells, B cells, NK cells, and macrophages (1). Cellular response to TNF-α is mediated through interaction with receptors TNF-R1 and TNF-R2 and results in activation of pathways that favor both cell survival and apoptosis depending on the cell type and biological context. Activation of kinase pathways (including JNK, Erk1/2, p38 MAPK, and NF-κB) promotes the survival of cells, while TNF-α-mediated activation of caspase-8 leads to programmed cell death (1,2). TNF-α plays a key regulatory role in inflammation and host defense against bacterial infection, notably Mycobacterium tuberculosis (3).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting

Background: Small ubiquitin-related modifier 1, 2 and 3 (SUMO-1, -2 and -3) are members of the ubiquitin-like protein family (1). The covalent attachment of the SUMO-1, -2 or -3 (SUMOylation) to target proteins is analogous to ubiquitination. This post-translational modification is a reversible, multi-step process that is initiated by cleaving a precursor protein to a mature protein. Mature SUMO-1, -2 or -3 is then linked to the activating enzyme E1, conjugated to E2 and in conjunction with E3, SUMO-1, -2 or -3 is ligated to the target protein (2). Ubiquitin and the individual SUMO family members are all targeted to different proteins with diverse biological functions. Ubiquitin predominantly regulates degradation of its target (1). In contrast, SUMO-1 is conjugated to RanGAP, PML, p53 and IκB-α to regulate nuclear trafficking, formation of subnuclear structures, regulation of transcriptional activity and protein stability (3-7). SUMO-2/-3 forms poly-(SUMO) chains, is conjugated to topoisomerase II and APP, regulates chromosomal segregation and cellular responses to environmental stress, and plays a role in the progression of Alzheimer disease (8-11).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunofluorescence (Frozen), Immunoprecipitation, Western Blotting

Background: The endocannabinoid system consists of the cannabinoid receptors, CB1 and CB2 receptors, the enzymes that produce and degrade the endogenous cannabinoid ligands (such as FAAH, DAG lipases, and MAG lipase), and the endocannabinoid ligands derived from the metabolism of arachidonic acid, 2-arachidonoylglycerol (2-AG) and anandamide (1-3). CB1 receptor belongs to the superfamily of G protein-coupled receptors (GPCRs) and harbors a large N-terminal extracellular domain, seven transmembrane domains, and a C-terminal intracellular tail. CB1 receptor is coupled to the Gai/o subunit of the G protein which inhibits adenylyl cyclases and regulates calcium and potassium ion channels (4). CB1 receptor is one of the most abundant GPCRs in the central nervous system. It has been show to play critical roles in the wiring of the brain during development (5), in neuronal plasticity (6), analgesia, drug abuse and metabolic homeostasis (7). In addition, CB1 receptor has been shown to interact with other GPCRs, to give rise to novel pharmacological and signaling heteromers with implication in diseases (8,9).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Voltage gated sodium channels are composed of a large alpha subunit and auxiliary beta subunits. The alpha subunit has 4 homologous domains, with each domain containing 6 transmembrane segments. These segments function as the voltage sensor and sodium permeable pore. Upon change of membrane potential, the sodium channel is activated, which allows sodium ions to flow through (1,2). When associated with beta subunits or other accessory proteins, the alpha subunit is regulated at the level of cell surface expression, kinetics, and voltage dependence (3,4).There are 9 mammalian alpha subunits, named Nav1.1-Nav1.9 (5). These alpha subunits differ in tissue specificity and biophysical functions (6,7). Seven of these subunits are essential for the initiation and propagation of action potentials in the central and peripheral nervous system while Nav1.4 and Nav1.5 are mainly expressed in skeletal muscle and cardiac muscle (8,9). Mutations in these alpha channel subunits have been identified in patients with epilepsy, seizure, ataxia, sensitivity to pain, and cardiomyopathy (reviewed in 10).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunofluorescence (Frozen), Immunoprecipitation, Western Blotting

Background: Contactin-associated protein 1 (Caspr) is a membrane protein that is an essential component of the paranodal junctions in the peripheral and central nervous systems (PNS and CNS, respectively). Caspr is part of the Neurexin family of proteins and is also known as Neurexin IV, Paranodin, and Cntnap1. Caspr forms a complex, via its extracellular domain, with contactin at paranodal junctions of the axon (1, 2). Paranodal junctions are specialized junctions in the axon that are formed between the axolemma and the paranodal loops of myelinating glia. Paranodal structures are critical for salutatory conduction in the PNS and CNS. In the absence of Caspr, Caspr knockout mice exhibit mislocalization of other paranodal junction proteins, including contactin and neurofascin (3). Knockout mice also exhibit reduced nerve conduction velocities, as well as behavior defects consistent with abnormal nerve conduction. Therefore, Caspr is a critical component of a protein complex that is likely central to paranodal junction formation and maintenance.