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Human RUNX1 / AML1 ELISA Kit (RMEK-0152866)

Cat. No.: RMEK-0152866

Category: ELISA Kits

INQUIRY 1 x 96 tests
Human RUNX1 / AML1 ELISA kit is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of Human RUNX1 / AML1 protein in human cell culture extracts. The technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time.

Product Features

Species Reactivity Human
Detection Method Colorimetric
Assay Duration One step assay
Assay Time 1.5 h
Assay Type Sandwich (quantitative)
Precision Intra-Assay-Extract-8-3.9%; Inter-Assay-Extract-3-6.4%
Sensitivity 41.73 pg/mL
Range 195.31 pg/mL - 12500 pg/mL
Sample Type Cell Lysate
Recovery Cell Lysate-90-89% - 93%
Key Features One-wash 90 minute protocol; Sensitivity: 41.73 pg/mL; Range: 195.31 pg/mL - 12500 pg/mL; Sample type: Cell Lysate; Detection method: Colorimetric; Assay type: Sandwich (quantitative); Reacts with: Human

Target Information

Target Symbol RUNX1 / AML1
Function CBF binds to the core site, 5'-PYGPYGGT-3', of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL-3 and GM-CSF promoters. The alpha subunit binds DNA and appears to have a role in the development of normal hematopoiesis. Isoform AML-1L interferes with the transactivation activity of RUNX1. Acts synergistically with ELF4 to transactivate the IL-3 promoter and with ELF2 to transactivate the mouse BLK promoter. Inhibits MYST4-dependent transcriptional activation.
Cellular Localization Nucleus.
Domain A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes.
Post-transcriptional Modifications Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with MYST3.Methylated.
Involvement in Disease A chromosomal aberration involving RUNX1/AML1 is a cause of M2 type acute myeloid leukemia (AML-M2). Translocation t(8; 21)(q22; q22) with RUNX1T1. A chromosomal aberration involving RUNX1/AML1 is a cause of therapy-related myelodysplastic syndrome (T-MDS). Translocation t(3; 21)(q26; q22) with EAP or MECOM. A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelogenous leukemia (CML). Translocation t(3; 21)(q26; q22) with EAP or MECOM. A chromosomal aberration involving RUNX1/AML1 is found in childhood acute lymphoblastic leukemia (ALL). Translocation t(12; 21)(p13; q22) with TEL. The translocation fuses the 3'-end of TEL to the alternate 5'-exon of AML-1H. A chromosomal aberration involving RUNX1 is found in acute leukemia. Translocation t(11,21)(q13; q22) that forms a MACROD1-RUNX1 fusion protein. Defects in RUNX1 are the cause of familial platelet disorder with associated myeloid malignancy (FPDMM). FPDMM is an autosomal dominant disease characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukemia. A chromosomal aberration involving RUNX1/AML1 is found in therapy-related myeloid malignancies. Translocation t(16; 21)(q24; q22) that forms a RUNX1-CBFA2T3 fusion protein. A chromosomal aberration involving RUNX1/AML1 is a cause of chronic myelomonocytic leukemia. Inversion inv(21)(q21; q22) with USP16.

Storage & Shipping

Storage Store at 2-8°C
Shipping Gel Packs
Stability The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition.

For research use only. Not for clinical use.