Pathways

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro. It is administered intravenously, and can act to decrease platelet aggregation for up to two days after administration. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of platelets. In the vein, Abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion.

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro. It is administered intravenously, and can act to decrease platelet aggregation for up to two days after administration. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of platelets. In the vein, Abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion.

Abciximab (also known as c7E3 Fab) is integrin (integrin alpha-IIb and integrin beta-3) receptor antagonist. Binding of abciximab to integrin receptor will block any large molecule to attach on the receptor, which will lead to block any associated signal transduction pathways.

Abciximab or Abcixifiban is a platelet aggregation inhibitor drug sold under the name ReoPro (also called c7E3 Fab as it is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3). It can decrease platelet aggregation for up to two days after administration, which is intravenous. Abciximab is an antigen binding fragment that targets glycoprotein IIb/IIIa receptors on the outer membrane of human platelets. It acts as an integrin (integrin alpha-IIb and integrin beta-3) receptor antagonist - thus, binding of abciximab to integrin receptor will block any large molecule to attach on the receptor, which will lead to block any associated signal transduction pathways: in this case, those involved in platelet aggregation are inhibited as fibrinogen and other adhesive molecules are blocked by abciximab. In the vein, abciximab causes a conformational change in the integrins on the surface of activated platelets. This prevents the binding of fibrinogen to these integrins, which in turn prevents the platelets from being held together by these fibrinogen fibres. The conformational change also prevents the binding of von Willebrand factor to the platelets, which also prevents aggregation and adhesion. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. It also blocks the Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. Altogether, abciximab increases bleeding time when administered. It has an initial plasma half-life of less than ten minutes and a second phase half-life of about half an hour, likely related to GPIIb/IIIa binding kinetics; however, it may occupy receptors for weeks due to its strong affinity. Abciximab is commonly used in the clinic during coronary artery procedures to prevent clotting during surgery.

Abscisic acid biosynthesis is a pathway that begins in the chloroplast and ends in the cytosol by which violaxanthin becomes abscisic acid, a plant hormone that plays a role in many plant developmental processes, including bud dormancy . First, neoxanthin synthase catalyzes the opening of the violaxanthin epoxide ring to form neoxanthin. Second, a yet unidentified neoxanthin isomerase is theorized to isomerize neoxanthin to 9'-cis-neoxanthin. Third, 9-cis-epoxycarotenoid dioxygenase (NCED) uses oxygen to cleave 9'-cis-neoxanthin to form xanthoxin and C25-allenic-apo-aldehyde. This enzyme requires Fe2+ as a cofactor. Next, a xanthoxin transporter is theorized to export xanthoxin from the chloroplast into the cytosol to continue abscisic acid biosynthesis, but it has yet to be discovered. Fourth, xanthoxin dehydrogenase, located in the cytosol, catalyzes the conversion of xanthoxin and NAD to abscisic aldehyde, NADH, and a proton with the help of a molybdenum cofactor (MoCo). Fifth, abscisic-aldehyde oxidase converts abscisic aldehyde, water, and oxygen into hydrogen peroxide, hydrogen ion, and abscisic acid.

Abscisic acid biosynthesis is a pathway that begins in the chloroplast and ends in the cytosol by which violaxanthin becomes abscisic acid, a plant hormone that plays a role in many plant developmental processes, including bud dormancy . First, neoxanthin synthase catalyzes the opening of the violaxanthin epoxide ring to form neoxanthin. Second, a yet unidentified neoxanthin isomerase is theorized to isomerize neoxanthin to 9'-cis-neoxanthin. Third, 9-cis-epoxycarotenoid dioxygenase (NCED) uses oxygen to cleave 9'-cis-neoxanthin to form xanthoxin and C25-allenic-apo-aldehyde. This enzyme requires Fe2+ as a cofactor. Next, a xanthoxin transporter is theorized to export xanthoxin from the chloroplast into the cytosol to continue abscisic acid biosynthesis, but it has yet to be discovered. Fourth, xanthoxin dehydrogenase, located in the cytosol, catalyzes the conversion of xanthoxin and NAD to abscisic aldehyde, NADH, and a proton with the help of a molybdenum cofactor (MoCo). Fifth, abscisic-aldehyde oxidase converts abscisic aldehyde, water, and oxygen into hydrogen peroxide, hydrogen ion, and abscisic acid.

Abscisic acid glucose ester metabolism is a pathway that begins in the chloroplast and enters the cytosol and endoplasmic reticulum body by which violaxanthin becomes abscisic acid glucose ester, synthesizing abscisic acid in the process. Abscisic acid glucose ester synthesis and reformation back to abscisic acid provides a mechanism for precisely controlling abscisic acid concentration (quickly removing and adding abscisic acid when required). First, neoxanthin synthase catalyzes the opening of the violaxanthin epoxide ring to form neoxanthin. Second, a yet unidentified neoxanthin isomerase is theorized to isomerize neoxanthin to 9'-cis-neoxanthin. Third, 9-cis-epoxycarotenoid dioxygenase (NCED) uses oxygen to cleave 9'-cis-neoxanthin to form xanthoxin and C25-allenic-apo-aldehyde. This enzyme requires Fe2+ as a cofactor. Next, a xanthoxin transporter is theorized to export xanthoxin from the chloroplast into the cytosol to continue abscisic acid biosynthesis, but it has yet to be discovered. Fourth, xanthoxin dehydrogenase, located in the cytosol, catalyzes the conversion of xanthoxin and NAD to abscisic aldehyde, NADH, and a proton with the help of a molybdenum cofactor (MoCo). Fifth, abscisic-aldehyde oxidase converts abscisic aldehyde, water, and oxygen into hydrogen peroxide, hydrogen ion, and abscisic acid. Sixth, abscisic acid glucosyltransferase uses UDP to convert abscisic acid into abscisic acid glucose ester. Abscisic acid glucose ester can then be converted back to abscisic acid via abscisic acid glucose ester beta-glucosidase located in the endoplasmic reticulum body (coloured dark green in the image). Consequently, it is theorized that ABA-GE transporters are required for this enzyme to access its substrates from the cytosol.