Description: B2M (Beta-2-Microglobulin) has been genetically removed by CRISPR/Cas9 genome editing from THP-1 cells.

Description: CIITA (Class II Transactivator) has been genetically removed from THP-1 cells using CRISPR/Cas9 genome editing.

Description: This cell line is a double knockout of TCR (T Cell Receptor) and B2M (Beta-2-Microglobulin). First, the TRAC (T-Cell Receptor Alpha Constant) and the TRBC1 (T-Cell Receptor Beta Constant 1) domains of the TCRα/β chains were genetically removed by CRISPR/Cas9 genome editing from Jurkat cells to generate the TCR Knockout Jurkat cell Line (BPS Bioscience #78539). These TCR knockout cells were then used to generate a new cell line in which B2M was also genetically removed by CRISPR/Cas9 genome editing.

Description: The FCGR2A Knockout Jurkat cell line was generated by CRISPR/Cas9 genome editing to remove FCGR2A (CD32A), the gene encoding protein FcγRIIa (Fragment crystallizable gamma receptor II a, also known as FcGRIIa, Fc-gamma-RIIa, and CD32A).

Description: Both B2M (Beta-2-Microglobulin) and CIITA (Class II Transactivator) have been genetically removed from THP-1 cells using CRISPR/Cas9 genome editing.

Description: B2M (Beta-2-Microglobulin) has been genetically removed by CRISPR/Cas9 genome editing from NFAT Luciferase Reporter Jurkat cells. Expression of the firefly luciferase gene is driven by NFAT response elements located upstream of the minimal TATA promoter. Activation of the NFAT signaling pathway in these cells can be monitored by measuring luciferase activity.

Description: This cell line is a knockout of TCR (T Cell Receptor). The TRAC (T-Cell Receptor Alpha Constant) and TRBC1 (T-Cell Receptor Beta Constant 1) domains of the TCRα/β chains were genetically removed by CRISPR/Cas9 genome editing from recombinant Jurkat cells stably expressing the firefly luciferase gene under the control of NFAT response elements.This cell line has been functionally validated and does not respond to anti-CD3 agonist antibodies, as opposed to parental NFAT-Luciferase Reporter Jurkat cells (BPS Bioscience #60621).

Description: This cell line is a double knockout of TCR (T Cell Receptor) and B2M (Beta-2-Microglobulin). First, the TRAC (T-Cell Receptor Alpha Constant) and the TRBC1 (T-Cell Receptor Beta Constant 1) domains of the TCRα/β chains were genetically removed by CRISPR/Cas9 genome editing from NFAT Luciferase Reporter Jurkat cells to generate the TCR Knockout NFAT Luciferase Reporter Jurkat cell Line (BPS Bioscience #78556). These TCR knockout cells were used to generate a new cell line in which B2M was also genetically removed by CRISPR/Cas9 genome editing. _x000D_Expression of the firefly luciferase gene is driven by NFAT response elements located upstream of the minimal TATA promoter. Activation of the NFAT signaling pathway in these cells can be monitored by measuring luciferase activity. 

Description: The CRISPR/Cas9 Kinase Knockout Lentivirus Library (Array Format) targets 619 human kinases and pseudo-kinases.bpsbioscience.com/media/wysiwyg/Kinases/Kinase_Library_-_List_Kinases_Pseudokinases_06-15-2022.xlsx Download the table to view all available kinases. The Array consists of a series of vials, with each vial containing a mixture of integrating CRISPR/Cas9 lentiviral particles targeting 5 sgRNAs for a specific gene (1 vial per gene, 5 sgRNAs per gene). The Array also includes a total of 150 control sgRNAs that do not target any gene (combined into 30 vials containing 5 control sgRNAs per vial). Thus, the Array contains a total of 649 vials and 3,245 sgRNAs.The lentiviruses are replication incompetent, VSV-G pseudotyped lentiviral particles ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The SIN (self-inactivation) lentiviral backbone contains the Cas9 gene (Streptococcus pyogenes CRISPR associated protein 9) driven by an EF1a promoter, an sgRNA driven by a U6 promoter, and a puromycin selection marker.The lentiviruses integrate randomly into the cellular genome to express both Cas9 and the sgRNAs. Because the lentiviruses contain Cas9, they can be used in any target cell regardless of whether the cells already express Cas9. Puromycin selection ensures high expression of both Cas9 and the sgRNAs. Knockout efficiencies will depend on the cell type and the gene of interest. Stable CRISPR/Cas9 knockout cell lines can also be generated following limiting dilution.The library is delivered with a User Manual booklet.

Description:

Random Primers are a mixture of oligonucleotides representing all possible sequence for that size. Random Primers can be used to prime synthesis in oligo-labeling similar to using hexamers (1,2) and cDNA synthesis. Random prime labeling yields high specific activity labeled DNA probe which can be used for all southern, northern and in situ hybridization studies. Random Primers can be also used similar to using hexamers in cDNA synthesis in combination with oligo d(T) to yield more 5' end cDNA sequence. Recently random primers have been used to detect DNA polymorphism. These polymorphisms, simply detected as DNA segments which amplify from one parent but not the other, are inherited in a Mendelian fashion and can be used to construct genetic maps in a variety of species. The authors suggested that these polymorphisms be called RAPD (pronounced RAPID) makers, after Random Amplified Polymorphic DNA (3).

References 1. Feinberg, A.P. & Vogelstein, B. (1983) Anal. Biochem. 132:6-13. 2. Feinberg, A.P. & Vogelstein, B. (1984) Anal. Biochem. 137:266-267. 3. Williams J. G., Kubelik A.R., Livak K.J., Rafalski J.A. & Tingey S.V. (1990) Nucleic Acid Res. 18(22):6531-5.

Description: Monkeypox is a viral zoonosis (a virus transmitted to humans from animals) with symptoms very similar to those seen in the past in smallpox patients, although it is clinically less severe. It is caused by the monkeypox virus which belongs to the orthopoxvirus genus of the Poxviridae family. There are two clades of monkeypox virus: the West African clade and the Congo Basin (Central African) clade. The name monkeypox originates from the initial discovery of the virus in monkeys in a Danish laboratory in 1958. The first human case was identified in a child in the Democratic Republic of the Congo in 1970.