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Cat. No. | Product Name | Target | Signaling Pathways |
---|---|---|---|
TN3711 |
Corylifol C
|
ERK; EGFR; p38 MAPK; MEK | Angiogenesis; JAK/STAT signaling; MAPK; Tyrosine Kinase/Adaptors |
Corylifol C and, to a lesser extent, xanthoangelol are potent protein kinase inhibitors (inhibitory concentration 50% values for epidermal growth factor receptor (EGFR): 1.1 and 4.4 × 10(-6) μg/ml, respectively). |
Cat. No. | Product Name | Species | Expression System |
---|---|---|---|
TMPK-01450 |
HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi), Biotinylated
KRAS1,MHC,K-RAS4B,KRAS,CFC2,K-RAS... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. | |||
TMPK-01456 |
HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Tetramer Protein, Human, MHC (His & Avi)
KRAS2,NS,MHC,C-K-RAS,KRAS1,K-RAS2A,K-RAS2B... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. | |||
TMPK-01451 |
HLA-C 03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi)
NS3,K-RAS4A,K-Ras 2,NS,KRAS1,RASK2,MHC,KI-RAS,KRAS,... |
Human | HEK293 Cells |
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail. |