CD202b / TEK pTyr992 antibody Ab
- Known as:
- CD202b / TEK pTyr992 (anti-) Antibody
- Catalog number:
- 1488172
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CD202b / TEK pTyr992 antibody
Ask about this productRelated genes to: CD202b / TEK pTyr992 antibody Ab
- Gene:
- TEK NIH gene
- Name:
- TEK receptor tyrosine kinase
- Previous symbol:
- VMCM
- Synonyms:
- TIE2, TIE-2, VMCM1, CD202b
- Chromosome:
- 9p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2018-08-07
Related products to: CD202b / TEK pTyr992 antibody Ab
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- Little is known regarding the extent to which the barriers separating brain subcompartments lead to differential drug transport into these subcompartments and whether such differences impact the behavioral effects of drugs. Against this background, here we have adopted electrochemical aptamer-based (EAB) sensors, a seconds-resolved, in vivo molecular measurement tool, to two tasks. First, we have measured the pharmacokinetics associated with the anesthetic procaine crossing the blood-brain-barrier into the solid tissue of the hippocampus and crossing the blood-cerebrospinal fluid barrier into the lateral ventricle. Second, we have determined the extent to which procaine concentrations in these two subcompartments correlate with the behavioral response the drug elicits. Performing these studies, we find that, whereas the drug's elimination kinetics are effectively indistinguishable between the two subcompartments, penetration into the hippocampus is statistically significantly slower than into the lateral ventricle. The relationships between drug concentration and the resulting behavioral effect also differ significantly between the two subcompartments, with the correlation between concentration and drug-induced suppression of ambulatory behavior being stronger in the hippocampus than in the lateral ventricle. This difference presumably arises because hippocampal concentrations more accurately reflect procaine exposure at the drug's site of action. - Source: PubMed
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