The mechanism of molecular redundancy in autoimmune inflammation in the context of CD44 deficiency.
Molecular redundancy refers to the ability of genes to back up damaged genes or gene loss. Although this term is widely discussed in many scientific circles, the process is still ill-defined, as shown by reviewing examples from the literature. Exploring the collagen-induced arthritis model in the context of CD44 knockout mice, we suggest a mechanistic explanation for molecular redundancy that depends neither on upregulation of the compensating molecule nor on structural similarity between the original molecule and the replacement molecule. The backup process is dependent, however, on two key properties shared by the two molecules: ligand binding and support of cell trafficking.
Naor
David
D
The Lautenberg Center for General and Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel. naord@md.huji.ac.il
Nedvetzki
Shlomo
S
Assayag
Nathalie
N
Thurmond
Robin L
RL
Huang
Jing-Feng
JF
Turley
Eva A
EA
D000818:Animals; D001169:Arthritis, Experimental / Q000235:genetics; D002465:Cell Movement / Q000276:immunology / Q000502:physiology*; D024043:Collagen Type II / Q000378:metabolism; D004195:Disease Models, Animal; D005434:Flow Cytometry; D018960:Hyaluronan Receptors / Q000235:genetics* / Q000378:metabolism*; D007249:Inflammation / Q000276:immunology*; D008024:Ligands; D051379:Mice; D018345:Mice, Knockout; D018448:Models, Immunological
D024043:Collagen Type II; D018960:Hyaluronan Receptors; D008024:Ligands