CXCR2 (IL-8RB) is a seven-transmembrane G protein-coupled receptor whose physiological ligands include IL-8 (CXCL8) and growth related oncogene α (Gro-α; CXCL1). IL-8 and Gro-α are pro-inflammatory CXC chemokines that act as chemoattractants, especially for neutrophils, and promote angiogenesis. SB 225002 is a selective non-peptide inhibitor of CXCR2, inhibiting IL-8 binding to CXCR2 with an IC50 value of 22 nM.{17249} SB225002 inhibits neutrophil chemotaxis in response to IL-8 in vitro (IC50 = 20 nM) and blocks neutrophil margination induced by IL-8 in vivo (IC50 = 30 nM).{17249} Similarly, SB 225002 reduces neutrophil influx, the production of inflammatory mediators, and tissue damage in TNBS-induced colitis in mice.{17248}
A selective non-peptide inhibitor of CXCR2, inhibiting IL-8 binding to CXCR2 (IC50 = 22 nM)
Formal name: N-(2-bromophenyl)-N’-(2-hydroxy-4-nitrophenyl)-urea
Synonyms:
Molecular weight: 352.1
CAS: 182498-32-4
Purity: ≥95%
Formulation: A crystalline solid
Product Type|Biochemicals|Receptor Pharmacology|Antagonists||Research Area|Immunology & Inflammation|Gastric Disease|Ulcerative Colitis||Research Area|Immunology & Inflammation|Innate Immunity
The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
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The PtdIn phosphates play an important role in the generation and transduction of intracellular signals.{8344,4096,14518} PtdIns-(3,4,5)-P3-biotin is an affinity probe which allows the PIP3 to be detected through an interaction with the biotin ligand. This design allows PtdIns-(3,4,5)-P3-biotin to serve as a general probe for any protein with a high affinity binding interaction with inositol-(3,4,5)-triphosphate phospholipids, such as phosphatidylinositol 3-kinase, PTEN, or PH-domain-containing proteins.
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The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
Available on backorder
The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
Available on backorder