p63 does not function as a tumor suppressor and is rarely mutated in human cancer24. However, when p63 is overexpressed it functions as an oncogene by several mechanisms including: opposition of p53 function (Chen 1999), loss of E-cadherin expression 25 and enhancement of cell
survival pathways 26. In addition , Cancer cells are affected by ∆Np63 by several mechanisms, one of them is by encouraging the migratory behavior of cancer cells and the other way is by downing the
adhesion of the cells to each other27. On the other hand, the role of p 63 in developing cancers still needs more investigation. Many researchers have reported the association of ∆Np63 with some type of cancer. ...view middle of the document...
The basic core structure of any antibody is formed from a Heavy chain (55-77kDa) and a light chain (25kDa) (H2L2) figure ( ). Some isoforms come in pentaform (H2L2)5 and others in monomer form (H2L2). Both chains are joined by disulfide bonds. The number and the position of those bonds vary and they attribute to formation of five isoforms. These are IgG, IgA, IgM, IgE, IgD. The IgG is one of the imuunoglbline isoforms that is found in serum concentration of 3-20 mg/ml. it is half life in the serum 2-4 days. In addition it has FcR binding. This type of antibody comes in monomer form (H2L2) which makes it more diffusable in serum and extracellular fluid. It represents 75% of other antibodies in serum34. These features are very important for our selection of secondary antibodies type as it will be explained later.
D) Autoantibodies to ∆Np63:
1) Definition of Autoantibodies:
Is a deviation of a crucial and defensive physiological process, in place of immunoglobulin act in response to self- molecules. Thus Autoantibodies are formed against self tissues are considered as aberration of immune response toward its cells. Certainly, Autoimmune diseases are part of autoantibodies reaction, which means there are more autoantibodies than autoantibodies diseases 35.
Tolerance of selfantigens is established at early life stages; during embryogenesis the process of tolerance is initiated. At birth recognition of non self molecules by the immune system will start, however, the breakage of tolerance can happen and awakening of autoimmune reaction against self molecules can be presented. Several theories tried to explain it, the assumption of molecular mimicry is one of the theories tried to find an explanation to this sort of reaction. The similarities between an external antigen and self antigen may lead to make the autoimmune system identify self molecules and
react against it after the infection of that specific external molecule. Cunningham found The occurrence of rheumatic carditis and inflammatory heart disease, is a consequence of mimicry to the group A streptococcus36.
2) Types of Autoantibodies:
Based on the pathogenic behavior, two types of autoanitbodise can be named. Physiological Autoantibodies and pathological one. The physiological one is transient and not associated with certain disease
2) Clinical application of Autoantibodies Testing:
Autoantibodies can be detectable in patients with no clinical symptoms of any autoimmune diseases, the use if autoantibodise as an indicator for potentially candidate patients do certain disease has been widely used. Diabetes Mellitus is a good example for this use. Presence of autoantibodies to Langerhans islet cells, IA-2A and GAD-65, are widely acknowledge as a predictor for type one D.M. in addition, The high association between the presence of GAD-65 and IA-2A autoantibodies and the potential alteration of type II D.M to...