Often times the golgi has been described as the post office of the cell delivering proteins to appropriate areas of the cell. The golgi has another very important role of modifying sugars on specific parts of a protein.
When a protein is placed into the membranes these sugars identify the sections of the protein that are not to be in the cytosol. The parts of a transmembrane protein with sugars are on the outside of the cell or on the inside of an organelle. The complete removal of mannose sugars signals that the protein is to be secreted.
The sugar Galactose on the outside of red blood cells have evolved the important duty of participating in clotting. Called the "blood type antigen" these galactose proteins on RBC are similar to van willebrand factor protein which is involved with platelets. The Galactose mediates the adhesion of platelets and Red blood cells to sites of vascular damage.
Type O has the weakest level of clotting
Type B has medium level clotting
Type A has the strongest level of clotting (the easiest to bind)
Bacterias, mycobacterias, and yeasts like candida grab on to the surface of cells through sugars and have evolved a strong affinity for galactose. Obviously the ideal place to infect is where a cut is.
To combat infections our bodies have developed "lewis antigens" The sugar Fucose of "lewis antigens" is very similar to Galactose. Fucose is the decoy for Galactose. Lewis antigens are secreted into the fluids and lower the infection rate.
People who lack the genes for lewis antigens have increased rates of intestinal infections and higher rates of ulcers.
The opposite can be said for blood type antigens. Those with type A and B are at increased risk of infections.
(if you have type A hope that you have Lewis Antigens to be decoys)
This leads to some interesting contemplations: antibodies can have lactose and that changes the binding to Fc receptors.
Read an interesting article where the Fc domain of IgG antibodies have sialic acid residues and these sugars are responsible for the inflammation properties of IgG antibodies
https://www.chemistryworld.com/news/sugar-coated-antibody/3003810.article
Does the presence of lactose in antibodies match up with the antibodies directed against viruses? Does the altered Fc binding of the antibody tell the immune system that it is viral by not having lacose and having galactose instead?
Fucose, galactose, sialic and antibodies....the fucose antibodies activate NK
https://www.ncbi.nlm.nih.gov/pubmed/18566325
why is fucose on the antibody's Fc for NK ?
NK cells are involved when ER infecting polyomaviruses are involved. No proteins make it to the surface to present antigens if the ER is infected.
does fucose helps jagged-notch binding ?
http://www.pnas.org/content/111/20/7290.full
http://www.jbc.org/content/280/37/32133.full
Does high amounts of galactose represent other non ER viruses?
HIV, Fc and galactose
https://www.ncbi.nlm.nih.gov/pubmed/25160934
https://www.ncbi.nlm.nih.gov/pubmed/21041724
When a protein is placed into the membranes these sugars identify the sections of the protein that are not to be in the cytosol. The parts of a transmembrane protein with sugars are on the outside of the cell or on the inside of an organelle. The complete removal of mannose sugars signals that the protein is to be secreted.
The sugar Galactose on the outside of red blood cells have evolved the important duty of participating in clotting. Called the "blood type antigen" these galactose proteins on RBC are similar to van willebrand factor protein which is involved with platelets. The Galactose mediates the adhesion of platelets and Red blood cells to sites of vascular damage.
Type O has the weakest level of clotting
Type B has medium level clotting
Type A has the strongest level of clotting (the easiest to bind)
Bacterias, mycobacterias, and yeasts like candida grab on to the surface of cells through sugars and have evolved a strong affinity for galactose. Obviously the ideal place to infect is where a cut is.
To combat infections our bodies have developed "lewis antigens" The sugar Fucose of "lewis antigens" is very similar to Galactose. Fucose is the decoy for Galactose. Lewis antigens are secreted into the fluids and lower the infection rate.
People who lack the genes for lewis antigens have increased rates of intestinal infections and higher rates of ulcers.
The opposite can be said for blood type antigens. Those with type A and B are at increased risk of infections.
(if you have type A hope that you have Lewis Antigens to be decoys)
This leads to some interesting contemplations: antibodies can have lactose and that changes the binding to Fc receptors.
Read an interesting article where the Fc domain of IgG antibodies have sialic acid residues and these sugars are responsible for the inflammation properties of IgG antibodies
https://www.chemistryworld.com/news/sugar-coated-antibody/3003810.article
Does the presence of lactose in antibodies match up with the antibodies directed against viruses? Does the altered Fc binding of the antibody tell the immune system that it is viral by not having lacose and having galactose instead?
Fucose, galactose, sialic and antibodies....the fucose antibodies activate NK
https://www.ncbi.nlm.nih.gov/pubmed/18566325
why is fucose on the antibody's Fc for NK ?
NK cells are involved when ER infecting polyomaviruses are involved. No proteins make it to the surface to present antigens if the ER is infected.
does fucose helps jagged-notch binding ?
http://www.pnas.org/content/111/20/7290.full
http://www.jbc.org/content/280/37/32133.full
Does high amounts of galactose represent other non ER viruses?
HIV, Fc and galactose
https://www.ncbi.nlm.nih.gov/pubmed/25160934
https://www.ncbi.nlm.nih.gov/pubmed/21041724
Consider:
Fucose: lewis antigen decoy/ bacteria binds / in the antibody for polyomaviruses ...triggering nk
Galactose: clotting factor/ bacteria binds / in the antibody for other viruses HIV etc
Sialic: anti-inflammation when on antibody for bacteria or large infections / virus binds/ not on antibodies for viruses?
Example: sialic antibodies against T.cruzi
https://www.hindawi.com/journals/scientifica/2013/965856/
However....there are articles where they say the Fc closes and can not bind to the receptors with sialic acid?
So fucose deficient IgG bound FcR111A (the Fc receptor connected to NK activation) tighter!!
http://www.jbc.org/content/277/30/26733.full
What exactly is happening here?
Example: sialic antibodies against T.cruzi
https://www.hindawi.com/journals/scientifica/2013/965856/
However....there are articles where they say the Fc closes and can not bind to the receptors with sialic acid?
So fucose deficient IgG bound FcR111A (the Fc receptor connected to NK activation) tighter!!
http://www.jbc.org/content/277/30/26733.full
What exactly is happening here?
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