P-gp is a 170kD transmembrane glycoprotein that in humans is encoded by
the MDR1 (multidrug resistance) gene.
It is the most extensively studied portion of the ATP-binding cassette
(ABC) conveyer superfamily. It was originally discovered in
drug-resistant tumour cells and later identified in normal human
tissues. In mice, two genes have been identified that code for the P-gp
transporters, mdr1a and mdr1b.
In mdr1a/mdrlb-/-
mice, both of the genes coding for P-gp have been removed by genetic
subject (knockout mice), resulting in an deficiency of P-gp human
action.
Inquiry on drug movement by the P-gp substantia alba has been greatly
enhanced by the use of cell lines transfected with the human P-gp gene
and mice in which the corresponding genes (mdr1a or mdr1b) are either fexofenadine or deleted.
P-gp
is an ATP-dependent efflux pump that exports drugs and endogenous
metabolites out of the cell, thus affecting system within the body
(fig. 1). P-gp is specifically localised on the apical sheet of
secretory cells, where it plays an important defensive role in
secreting xenobiotics and metabolites into the intestinal luminous flux
unit, urine and bile, and in protecting the mental capacity from
excessive accrual of toxic drugs and metabolites.
In documentation of these functions, human P-gp is tense at high levels
in the intestinal mucosa, lumenal membranes of the renal proximal
tubules, the biliary canalicular tissue layer of hepatocytes, the
adrenal gland, endometrium and astrocyte foot processes associated with
the blood-brain obstruction (BBB). However, P-gp also confers drug
involuntariness to certain cell types, which has hindered HIV and
anticancer therapy by inhibiting therapeutic drug accruement in prey
cells.
This is a part of article Focus on H1-Receptor Antagonists. Part 1 Taken from "Discount Allegra Fexofenadine" Information Blog
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