|
hnf1a protein, zebrafish
|
C496491 |
|
|
abrine
|
C496492 |
|
|
tRNA, N-acetylphenylalanine-4-thiouridine-
|
C036610 |
|
|
gabalid
|
C036611 |
|
|
propionohydroxamic acid
|
C036612 |
|
|
bestrabucil
|
C036613 |
|
|
VDP protocol
|
C036614 |
|
|
bicuculline methobromide
|
C036615 |
|
|
etintidine
|
C036616 |
|
|
3-(5-((4-(methylsulfonyl)-1-piperazinyl)methyl)-1H-indole-2-yl)quinolin-2(1H)-one
|
C496486 |
|
|
salsolinol
|
C036617 |
|
|
HNF1A protein, human
|
C496487 |
|
|
2-di-n-propylamino-5,8-dimethoxytetralin
|
C036618 |
|
|
Hnf1a protein, mouse
|
C496488 |
|
|
idebenone
|
C036619 |
|
|
Hnf1a protein, rat
|
C496489 |
|
|
Receptor, Insulin
|
D011972 |
[A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE.
] |
|
Receptors, LDL
|
D011973 |
[Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.
] |
|
Receptors, LH
|
D011974 |
[Those protein complexes or molecular sites on the surfaces and cytoplasm of gonadal cells that bind luteinizing or chorionic gonadotropic hormones and thereby cause the gonadal cells to synthesize and secrete sex steroids. The hormone-receptor complex is internalized from the plasma membrane and initiates steroid synthesis.
] |
|
Receptors, Mitogen
|
D011975 |
[Glycoprotein molecules on the surface of B- and T-lymphocytes, that react with molecules of antilymphocyte sera, lectins, and other agents which induce blast transformation of lymphocytes.
] |
