ELISA/assay

Rat Antioncogene p16 protein ELISA Kit

MBS721562

96 Strip Wells

675 USD

ELISA Kit

Rat Antioncogene p16 protein ELISA Kit

Antioncogene p16 protein

p16, partial; Cyclin-dependent kinase inhibitor 2A, isoforms 1/2/3; cyclin-dependent kinase inhibitor 2A; CDK4 inhibitor p16-INK4; multiple tumor suppressor 1; cell cycle negative regulator beta; cyclin-dependent kinase 4 inhibitor A; cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4); cyclin-dependent kinase inhibitor 2A; Cyclin-dependent kinase 4 inhibitor A; CDK4I; Multiple tumor suppressor 1; MTS-1; p16-INK4a; p16-INK4; p16INK4A

p16

CDKN2A; CDKN2A; ARF; MLM; P14; P16; P19; CMM2; INK4; MTS1; TP16; CDK4I; CDKN2; INK4A; MTS-1; P14ARF; P19ARF; P16INK4; P16INK4A; P16-INK4A; CDKN2; MTS1; CDK4I; MTS-1; p16-INK4; p16INK4A

CD2A1_HUMAN

Rat

This assay has high sensitivity and excellent specificity for detection of ?1-MG. No significant cross-reactivity or interference between ?1-MG and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ?1-MG 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. Intended Uses: This ?1-MG ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat ?1-MG. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Sensitivity: The sensitivity in this assay is 1.0 ng/mL.

Cancer

Principle of the assay: ?1-MG ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-?1-MG antibody and an ?1-MG-HRP conjugate. The assay sample and buffer are incubated together with ?1-MG-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 ?1-MG concentration since ?1-MG from samples and ?1-MG-HRP conjugate compete for the anti-?1-MG antibody binding site. Since the number of sites is limited, as more sites are occupied by ?1-MG from the sample, fewer sites are left to bind ?1-MG-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ?1-MG concentration in each sample is interpolated from this standard curve.

89355819

ABD72255.1

8,731 Da

Apoptosis Pathway 198797!!Apoptosis Modulation And Signaling Pathway 198822!!Bladder Cancer Pathway 83115!!Bladder Cancer Pathway 527!!Cell Cycle Pathway 530733!!Cell Cycle, Mitotic Pathway 105765!!Cell Cycle Pathway 198811!!Cell Cycle Pathway 83054!!Cell Cycle Pathway 463!!Cellular Senescence Pathway 905991

This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. [provided by RefSeq, Sep 2012]

96 Strip Wells

675 USD