2-Palmitoyl glycerol (2-PG) has been isolated along with the potent endocannabinoid 2-arachidonoyl glycerol (2-AG) from various tissues.{9610} Although 2-PG displays no intrinsic agonist activity on CB1 or CB2 receptors, it does potentiate the ability of 2-AG to inhibit adenylyl cyclase. 2-PG also potentiates the analgesic, hypokinetic, and anxiolytic effects of 2-AG in mice. This “entourage” effect has been attributed to the ability of compounds such as 2-PG to inhibit reuptake and/or compete with the active endocannabinoids for access to inactivating enzymes such as FAAH and monoglyceride lipase.{10671,9575} Palmitoyl serinol is a stable analog of 2-PG bearing an amide linkage in place of the labile glyceryl ester. This has the potential to enhance its “entourage” activities as a result of a prolonged in vivo half-life. Palmitoyl serinol is also an analog of C-16 ceramide. Incubation of neuroblastoma cells with palmitoyl serinol causes apoptosis with an IC50 of approximately 80 µM.{8954,10417}
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A stable analog of 2-PG bearing an amide linkage in place of the labile glyceryl ester which endows it with a prolonged in vivo half-life; also an analog of C-16 ceramide; causes apoptosis (IC50 = 80 µM) when incubated with neuroblastoma cells
Formal name: N-[2-hydroxy-1-(hydroxymethyl)ethyl]-hexadecanamide
Synonyms:
Molecular weight: 329.5
CAS: 126127-31-9
Purity: ≥98%
Formulation: A crystalline solid
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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Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression and are therefore promising targets for cancer therapy. (R)-Roscovitine is a potent inhibitor of Cdk2/cyclin E with an IC50 value of 0.1 µM.{14988} It also inhibits Cdk7/cyclin H, Cdk5/p35, and cell division cycle (cdc)/cyclin B with IC50 values of 0.49, 0.16, and 0.65 µM, respectively.{14987,14988,14991} (R)-Roscovitine inhibits the growth of rapidly proliferating cells with an average IC50 value of 15.2 µM against a panel of 19 human tumor cell lines.{14988} In murine models of polycystic kidney disease, (R)-roscovitine effectively inhibited disease progression at doses of 50-100 mg/kg.{14564}
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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}
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