Specifications
- Assay duration:Multiple steps
- Assay Type (ELISA with LOV):Sandwich
- Conjugate ELISA:Biotin
- Format:Pre-coated
- Host:Rabbit
- Primary antibody reactivity:Mouse
- Target protein:DDIT3
- Size:1 kit
- Sample Type:Tissue homogenates, cell lysates and other biological fluids
- Cross Reactivity:No significant cross-reactivity or interference between DNA Damage Inducible Transcript 3 (DDIT3) and analogues was observed
- Detection Method:Colorimetric
- Time to Results:3 h
- Shelf Life:12 Months
- Detection Range:0.156 - 10 ng/ml
- Storage Temperature:4 °C for one month (frequent use), −20 °C for one year
- Sample Volume:100 µl
- Sensitivity:0.060 ng/ml
- Regulatory Status:RUO
- Cat. No.:MSPP-SEJ282MU
- No. of tests:96 wells
Specifications
About this item
This assay has high sensitivity and excellent specificity for detecting Mouse DDIT3 (DNA Damage Inducible Transcript 3). The assay range is from 0.156 to 10 ng/ml (Sandwich kit) with a sensitivity of 0.060 ng/ml. There is no detectable cross-reactivity with other relevant proteins. Activity loss rate and accelerated stability test ect have been conducted to guarantee the best performance of the products after long storage and delivery.
- High sensitivity and specificity
- Perfect reproducibility and consistency across batches
- Quality control with three-level inspections
- Wide range of targets/species available
- Intra-assay: CV<10%; Inter-assay: CV<12%
The DDIT3 gene shows a high level of conservation in both the structural and regulatory regions to the previously described hamster gene. The human and hamster proteins share 91% amino acid identity. CHOP serves as a dominant-negative inhibitor of the transcription factors C/EBP and LAP. Bacterially expressed CHOP inhibited the DNA-binding activity of C/EBP and LAP by forming heterodimers that could not bind DNA.Chop also activated Ero1-alpha (ERO1L), which encodes an ER oxidase. Consequently, the ER of stressed Chop -/- cells was hypooxidized relative to the ER of stressed wildtype cells. Pharmacologic and genetic manipulations promoting a hypooxidized ER reduced abnormal high molecular mass protein complexes and protected cells from the lethal consequences of ER stress.