Dsred2 er

Manufactured by Takara Bio

The DsRed2-ER is a fluorescent protein product from Takara Bio. It is derived from the Discosoma species red fluorescent protein and is engineered to localize to the endoplasmic reticulum of cells.

Automatically generated - may contain errors

Lab products found in correlation

Dsred2 mito, by Takara Bio (1 mentions) Lsm 510 meta multiphoton confocal microscope, by Zeiss (1 mentions) Lipofectamine rnaimax, by Thermo Fisher Scientific (1 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (1 mentions) β gal, by Applied Biological Materials (1 mentions)

Close spelling variants of this product

DsRed2

2 protocols using dsred2 er

Immunolocalization of STING and TBK1 in HeLa Cells

Check if the same lab product or an alternative is used in the 5 most similar protocols

HeLa cells were seeded on coverslips in 6-well plates the day before transfection and cultured for 24 h. Plasmids of interest were transfected for 36 h before cells were fixed with 4% paraformaldehyde. For immunostaining, cells were first blocked with 5% BSA for 1 h followed by 5-min permeabilization with 0.2% Triton X-100. Cells were then incubated with primary antibody (1:200; mouse anti-HA for STING-β and mouse anti-FLAG for TBK1) overnight at 4°C. After washing with 1× PBS for three times, goat anti-mouse IgG conjugated to TRITC (1:200; Zymed) was added and incubated for 1 h. After washing with 1× PBS for three times, the coverslips were mounted onto the slides for observation using Carl Zeiss LSM 510 META Multiphoton Confocal Microscope. DsRed2-ER and DsRed2-Mito (Clontech) served as ER and mitochondrial markers.

Wang P.H., Fung S.Y., Gao W.W., Deng J.J., Cheng Y., Chaudhary V., Yuen K.S., Ho T.H., Chan C.P., Zhang Y., Kok K.H., Yang W., Chan C.P, & Jin D.Y. (2018). A novel transcript isoform of STING that sequesters cGAMP and dominantly inhibits innate nucleic acid sensing. Nucleic Acids Research, 46(8), 4054-4071.

+ Open protocol

+ Expand

Plasmid Characterization and Cardiomyocyte Manipulation

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

The DsRed2-ER (^#632409) plasmid was purchased from Clontech Laboratories, Inc. (Mountain View, CA). GFP-Fundc1Δ7-48 mutation plasmid was generated using Quikchange ӀӀ Site-directed Mutagenesis Kit (Agilent Cat: 200523). The procedure was followed with the company protocol. The GFP-Fundc1 plasmid (Origene Cat: RG208211) was used to delete region 7-48. The resulting plasmid was sequenced and confirmed with T7 primer. Cardiomyocytes were transfected with plasmids using Lipofectamine 2000 (^#11668-019, Life Technologies, Carlsbad, CA), according to the manufacturer’s protocol.
Fundc1 siRNA (^#sc-145273) was purchased from Santa Cruz Biotechnology, Inc. (Dallas, Texas). Itpr2 siRNA (^#n435663) was purchased from Life Technologies. For gene silencing of Fundc1 or Itpr2, cardiomyocytes were transfected with 10 μmol/L siRNA using Lipofectamine^®RNAiMAX (^#13778150, Life Technologies, Carlsbad, CA) according to the instructions provided by the supplier.
The mouse neonatal cardiomyocytes or H9c2 myoblasts were infected with adenovirus encoding Fundc1 (^#197503A and ^#281786A, Applied Biological Materials Inc., Canada) in normal culture medium for 48 h. An adenoviral vector encoding beta-galactosidase (β-Gal) (^#000197A, Applied Biological Materials Inc., Canada) was used as a control. Adenovirus encoding constitutively active Ampk mutants (ad-Ampk-CA) was generated as described earlier^{30 (link)}.

Wu S., Lu Q., Ding Y., Wu Y., Qiu Y., Wang P., Mao X., Huang K., Xie Z, & Zou M.H. (2019). Hyperglycemia-driven Inhibition of AMP-Activated Protein Kinase α2 Induces Diabetic Cardiomyopathy by Promoting Mitochondria-associated Endoplasmic Reticulum Membranes in vivo. Circulation, 139(16), 1913-1936.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!