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Id2 Mouse siRNA Oligo Duplex (Locus ID 15902)

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SKU
SR402424
Id2 (Mouse) - 3 unique 27mer siRNA duplexes - 2 nmol each
  $518.00
In Stock*

Frequently Bought Together (3)

TT320001 siTran 2.0 siRNA transfection reagent (0.5ml)
500 ul
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SR30002 Trilencer-27 Fluorescent-labeled transfection control siRNA duplex - 1 nmol
1 nmol
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TT300007S A non-viral, non-electroporation, non-liposomal transfection kit using engineered mammalian proteins, tailored for high-efficiency delivery into a wide range of primary cells and difficult to transfect cell lines such as immune cells, stem cells, and neuronal cells.
20 ul
$265.00

Other products for "Id2 or NM_010496"

Specifications
Specifications
Product Data
Purity HPLC purified
Quality Control Tested by ESI-MS
Sequences Available with shipment
Components
Id2 (Mouse) - 3 unique 27mer siRNA duplexes - 2 nmol each (Locus ID 15902)
Included - SR30004, Trilencer-27 Universal Scrambled Negative Control siRNA Duplex - 2 nmol
Included - SR30005, RNAse free siRNA Duplex Resuspension Buffer - 2 ml
Stability One year from date of shipment when stored at -20°C.
Shipping Ambient
# of Transfections Approximately 330 transfections/2nmol in 24-well plate under optimized conditions (final conc. 10 nM).
Note Single siRNA duplex (10nmol) can be ordered.
Reference Data
RefSeq NM_010496
UniProt ID P41136
Synonyms AI255428; bHLHb26; C78922; Idb2
Summary Transcriptional regulator (lacking a basic DNA binding domain) which negatively regulates the basic helix-loop-helix (bHLH) transcription factors by forming heterodimers and inhibiting their DNA binding and transcriptional activity. Implicated in regulating a variety of cellular processes, including cellular growth, senescence, differentiation, apoptosis, angiogenesis, and neoplastic transformation. Inhibits skeletal muscle and cardiac myocyte differentiation. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer. Restricts the CLOCK and ARNTL/BMAL1 localization to the cytoplasm. Plays a role in both the input and output pathways of the circadian clock: in the input component, is involved in modulating the magnitude of photic entrainment and in the output component, contributes to the regulation of a variety of liver clock-controlled genes involved in lipid metabolism.UniProtKB/Swiss-Prot Function
Performance Guaranteed OriGene guarantees that at least two of the three Dicer-Substrate duplexes in the kit will provide at least 70% or more knockdown of the target mRNA when used at 10 nM concentration by quantitative RT-PCR when the TYE-563 fluorescent transfection control duplex (cat# SR30002) indicates that >90% of the cells have been transfected and the HPRT positive control (cat# SR30003) provides 90% knockdown efficiency.

For non-conforming siRNA, requests for replacement product must be made within ninety (90) days from the date of delivery of the siRNA kit. To arrange for a free replacement with newly designed duplexes, please contact Technical Services at techsupport@origene.com. Please provide your data indicating the transfection efficiency and measurement of gene expression knockdown compared to the scrambled siRNA control (quantitative RT-PCR data required).
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Documents
Resources

file-alt Citations

Id4 promotes the elimination of the pro-activation factor Ascl1 to maintain quiescence of adult hippocampal stem cells
Blomfield, Rocamonde, Masdeu et al
Elife (2019) 8 DOI: 10.7554/eLife.48561
AI Summary: In this study, OriGene's HPRT-targeting siRNA was used as a positive control to validate the efficiency of siRNA-mediated gene silencing in neural stem cell experiments investigating the role of Id4 in maintaining stem cell quiescence.
Snippet: … NSCs were transfected with a cocktail of three siRNAs at 20 nM each, or 60 nM control scrambled siRNA, or 60 nM HPRT-targeting siRNA as a positive control (Origene). To silence Id4 in combination with Id1, Id2 or Id3, 30 nM of Id4 ‘A’ siRNA was co-transfected with 30 nM of siRNA ‘A’ targeting Id1, 2 or 3. …
FigureFigureFigure
Showing 1-1 of 1 papers.
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