ELISA/assay

Canine Caspase-3 ELISA Kit

MBS735215

48-Strip-Wells

470 USD

ELISA Kit

Canine Caspase-3 ELISA Kit

Caspase-3

caspase-3 preproprotein; Caspase-3; caspase-3; CASP-3; CPP-32; apopain; procaspase3; protein Yama; PARP cleavage protease; cysteine protease CPP32; SREBP cleavage activity 1; caspase 3, apoptosis-related cysteine protease; caspase 3, apoptosis-related cysteine peptidase; Apopain; Cysteine protease CPP32; CPP-32; Protein Yama; SREBP cleavage activity 1; SCA-1

caspase-3

CASP3; CASP3; CPP32; SCA-1; CPP32B; CPP32; CASP-3; CPP-32; SCA-1

CASP3_HUMAN

Canine

This assay has high sensitivity and excellent specificity for detection of CASPASE-3. No significant cross-reactivity or interference between CASPASE-3 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CASPASE-3 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 0.1 ng/mL.

Intended Uses: This CASPASE-3 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Canine CASPASE-3. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cell Biology

Principle of the assay: CASPASE-3 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CASPASE-3 antibody and an CASPASE-3-HRP conjugate. The assay sample and buffer are incubated together with CASPASE-3-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the CASPASE-3 concentration since CASPASE-3 from samples and CASPASE-3-HRP conjugate compete for the anti-CASPASE-3 antibody binding site. Since the number of sites is limited, as more sites are occupied by CASPASE-3 from the sample, fewer sites are left to bind CASPASE-3-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CASPASE-3 concentration in each sample is interpolated from this standard curve.

14790119

NP_004337.2

NM_004346.3

31,608 Da

AGE/RAGE Pathway (698754); Activation Of DNA Fragmentation Factor Pathway (105683); Activation Of Caspases Through Apoptosome-mediated Cleavage Pathway (105672); Alpha6-Beta4 Integrin Signaling Pathway (198807); Alzheimer's Disease Pathway (83097); Alzheimer's Disease Pathway (509); Alzheimers Disease Pathway (672448); Amoebiasis Pathway (167324); Amoebiasis Pathway (167191); Amyotrophic Lateral Sclerosis (ALS) Pathway (920975)

This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. This protein cleaves and activates caspases 6, 7 and 9, and the protein itself is processed by caspases 8, 9 and 10. It is the predominant caspase involved in the cleavage of amyloid-beta 4A precursor protein, which is associated with neuronal death in Alzheimer's disease. Alternative splicing of this gene results in two transcript variants that encode the same protein. [provided by RefSeq, Jul 2008]

CASP3: Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a 216-Asp- -Gly-217 bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop- helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage. Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 17 kDa (p17) and a 12 kDa (p12) subunit. Interacts with BIRC6/bruce. Highly expressed in lung, spleen, heart, liver and kidney. Moderate levels in brain and skeletal muscle, and low in testis. Also found in many cell lines, highest expression in cells of the immune system. Inhibited by isatin sulfonamides. Belongs to the peptidase C14A family. Protein type: Motility/polarity/chemotaxis; EC 3.4.22.56; Protease; Apoptosis. Chromosomal Location of Human Ortholog: 4q34. Cellular Component: nucleoplasm; plasma membrane; nucleus; cytosol. Molecular Function: cyclin-dependent protein kinase inhibitor activity; peptidase activity; protein binding; cysteine-type endopeptidase activity; aspartic-type endopeptidase activity. Biological Process: extracellular matrix organization and biogenesis; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; apoptosis; heart development; negative regulation of activated T cell proliferation; negative regulation of B cell proliferation; proteolysis; regulation of caspase activity; neuron differentiation; extracellular matrix disassembly; sensory perception of sound; B cell homeostasis; positive regulation of neuron apoptosis; response to wounding; erythrocyte differentiation; T cell homeostasis; DNA fragmentation during apoptosis; response to UV; cell structure disassembly during apoptosis; release of cytochrome c from mitochondria; cell fate commitment; negative regulation of cyclin-dependent protein kinase activity; keratinocyte differentiation; neuron apoptosis; induction of apoptosis via death domain receptors; caspase activation via cytochrome c; platelet formation; induction of apoptosis by oxidative stress; response to DNA damage stimulus; negative regulation of apoptosis

48-Strip-Wells

470 USD

96-Strip-Wells

675