Publications by authors named "S Sharoyan"

Fibronectin serves as a platform to guide and facilitate deposition of collagen and fibrillin microfibrils. During development of fibrotic diseases, altered fibronectin deposition in the extracellular matrix (ECM) is generally an early event. After this, dysregulated organization of fibrillins and fibrillar collagens occurs.

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Fibril formation by amyloidogenic proteins and peptides is considered the cause of a number of incurable diseases. One of the most known amyloid diseases is Alzheimer's disease (AD). Traditionally, amyloidogenic beta peptides Aβ40 and Aβ42 (Aβs) are considered as main causes of AD and the foremost targets in AD fight.

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The presence of citrullinated adenosine deaminase (ADA) was reported in the synovial fluids of rheumatoid arthritis individuals. This work reports the effects of ADA citrullination on the formation/stabilization of ADA complex with dipeptidyl peptidase IV (DPPIV). The electrophoretic mobility of in vivo citrullinated ADA was diminished compared to the native one.

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Compelling evidence suggests a crucial role of amyloid beta peptides (Aβ(1-40/42)) in the etiology of Alzheimer's disease (AD). The N-terminal truncation of Aβ(1-40/42) and their modification, e.g.

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Unlabelled: The aggregates of amyloid beta peptides (Aβs) are regarded as one of the main pathological hallmarks of Alzheimer's disease (AD). An imbalance between the rates of synthesis and clearance of Aβs is considered to be a possible cause for the onset of AD. Dipeptidyl peptidases II and IV (DPPII and DPPIV) are serine proteases removing N-terminal dipeptides from polypeptides and proteins with proline or alanine on the penultimate position.

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