Warning: The NCBI web site requires JavaScript to function. more...
An official website of the United States government
The .gov means it's official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site.
The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.
Binding affinity to CD14/MD2 (unknown origin) expressed in HEK-Blue cells co-expressing TLR4 assessed as inhibition of PHA-P-induced TLR4 signaling by measuring reduction in IL-8 secretion preincubated for 30 mins followed by PHA-P stimulation measured after overnight incubation by ELISA
Assay data:2 Active, 2 Tested
SummaryCompounds, ActivePubMed CitationRelated BioAssays by Target
Binding affinity to CD14/MD2 (unknown origin) expressed in HEK-Blue cells co-expressing TLR4 assessed as inhibition of LPS-induced TLR4 signaling by measuring reduction in IL-8 secretion preincubated for 30 mins followed by LPS stimulation measured after overnight incubation by ELISA
Binding affinity to CD14/MD2 in Balb/c mouse splenocytes assessed as inhibition of LPS-induced TLR4-MyD88 pathway by measuring reduction in TNFalpha expression at 1 to 10 uM preincubated for 30 mins followed by LPS stimulation for 5 hrs by qRT-PCR method
Binding affinity to CD14/MD2 in mouse RAW-Blue cells assessed as inhibition of LPS-induced TLR4 signaling preincubated for 30 mins followed by LPS stimulation measured after overnight incubation by secreted embryonic alkaline phosphatase reporter gene assay
Assay data:2 Tested
SummaryPubMed CitationRelated BioAssays by Target
Binding affinity to CD14/MD2 in human PBMC assessed as inhibition of LPS-induced TLR4 signaling by measuring decrease in IL-8 secretion at 1 to 10 uM preincubated for 30 mins followed by LPS stimulation for 18 hrs by ELISA
Binding affinity to CD14/MD2 in human PBMC assessed as inhibition of LPS-induced TLR4 signaling by measuring decrease in IL-6 secretion at 1 to 10 uM preincubated for 30 mins followed by LPS stimulation for 18 hrs by ELISA
Binding affinity to CD14/MD2 in human PBMC assessed as inhibition of LPS-induced TLR4 signaling by measuring decrease in TNFalpha secretion at 1 to 10 uM preincubated for 30 mins followed by LPS stimulation for 18 hrs by ELISA
Assay data:1 Active, 2 Tested
Binding affinity to CD14/MD2 (unknown origin) expressed in HEK-Blue cells co-expressing TLR4 assessed as inhibition of PHA-P-induced TLR4 signaling preincubated for 30 mins followed by PHA-P stimulation measured after overnight incubation by secreted embryonic alkaline phosphatase reporter gene assay
Binding affinity to CD14/MD2 (unknown origin) expressed in HEK-Blue cells co-expressing TLR4 assessed as inhibition of LPS-induced TLR4 signaling at 0.1 to 100 uM preincubated for 30 mins followed by LPS stimulation measured after overnight incubation by secreted embryonic alkaline phosphatase reporter gene assay
Assay data:3 Tested
Binding affinity to CD14/MD2 (unknown origin) expressed in HEK-Blue cells co-expressing TLR4 assessed as inhibition of LPS-induced TLR4 signaling preincubated for 30 mins followed by LPS stimulation measured after overnight incubation by secreted embryonic alkaline phosphatase reporter gene assay
Assay data:4 Active, 2 Activity ≤ 1 µM, 6 Tested
SummaryCompounds, ActiveCompounds, activity ≤ 1 µMPubMed CitationRelated BioAssays by Target
Activation of human TLR4/MD2 complex in mouse RAW264.7 cells assessed as induction of NFkappaB activation incubated for 18 hrs
Assay data:1 Active, 1 Tested
Inhibition of CD14 in mouse RAW264.7 cells at 20 uM by Western blotting analysis
Assay data:1 Tested
Activation of human TLR4/MD-2/CD14 transfected in HEK293 cells at 10 uM after 20 to 24 hrs by SEAP assay
Activation of mouse TLR4/MD-2/CD14 complex in C57BL/6 mouse BMDC cells assessed as NFkappaB activation by SEAP assay in presence of LPS-RS
Filters: Manage Filters
Your browsing activity is empty.
Activity recording is turned off.
Turn recording back on