6-keto prostaglandin F1α (6-keto PGF1α) is the inactive, non-enzymatic hydrolysis product of PGI2.{441,443} 6-keto PGF1α serves as a useful marker of PGI2 biosynthesis in vivo.{439} When [3H]-PGI2 is injected into healthy human males, 6.6% of the radioactivity is recovered from urine as [3H]-6-keto PGF1α.{439}
The inactive, non-enzymatic hydrolysis product of PGI2,
Formal name: 6-oxo-9α,11α,15S-trihydroxy-prost-13E-en-1-oic acid
Synonyms: 6-keto PGF1α
Molecular weight: 370.5
CAS: 58962-34-8
Purity: ≥98%
Formulation: A crystalline solid
Product Type|Biochemicals|Lipids|Prostaglandins||Research Area|Lipid Biochemistry|Cyclooxygenase Pathway
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 maintenance of embryonic stem cells in culture typically requires feeder cells and various exogenous factors found in serum. Murine embryonic stem (mES) cells can be maintained in the absence of feeder cells and serum but require the leukemia inhibitor factor (LIF) and bone morphogenic protein (BMP) to prevent differentiation and promote self-renewal. SC-1 is a small molecule activator of stem cell renewal that allows the propagation of OG2 mES cells for at least 10 passages in an undifferentiated state.{14533} The activity of SC-1 is mediated by the combined inhibition of RasGAP and ERK1 with Kd values of 98 and 212 nM, respectively.{14533} Inhibition of RasGAP increases Ras signaling via the PI3-kinase pathway which promotes self-renewal, whereas inhibition of ERK blocks differentiation.
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