TY - JOUR
T1 - Phage-displayed antibodies for the detection of glycated proteasome in aging cells
AU - Gonzalez-Dosal, Regina
AU - Sørensen, Morten Dræby
AU - Clark, Brian F.C.
AU - Rattan, Suresh I.S.
AU - Kristensen, Peter
PY - 2006/1/1
Y1 - 2006/1/1
N2 - Accumulation of posttranslationally damaged proteins during aging could explain the decline of cell performance with age. Nε- carboxymethyllysine (CML) is the major glycation product on damaged proteins, causing dysfunction and cross-linking. The proteasome, a multicatalytic degradation complex, is one of the pathways for eliminating damaged proteins, and thus regulating their accumulation within the cell. However, the proteinase activities of the proteasome decline during aging. This may be due to posttranslational modifications of the subunits forming the proteasome complex. Using phage display technology, we have selected 16 single-chain variable fragments (scFv) recognizing the CML-modified α7 subunit of the proteasome. Using one of them, Ab3, we have observed a five-fold increase of CML-α7 in old human skin fibroblasts in comparison with young fibroblasts and telomerase-immortalized bone marrow cells (hTERT-BMCs).
AB - Accumulation of posttranslationally damaged proteins during aging could explain the decline of cell performance with age. Nε- carboxymethyllysine (CML) is the major glycation product on damaged proteins, causing dysfunction and cross-linking. The proteasome, a multicatalytic degradation complex, is one of the pathways for eliminating damaged proteins, and thus regulating their accumulation within the cell. However, the proteinase activities of the proteasome decline during aging. This may be due to posttranslational modifications of the subunits forming the proteasome complex. Using phage display technology, we have selected 16 single-chain variable fragments (scFv) recognizing the CML-modified α7 subunit of the proteasome. Using one of them, Ab3, we have observed a five-fold increase of CML-α7 in old human skin fibroblasts in comparison with young fibroblasts and telomerase-immortalized bone marrow cells (hTERT-BMCs).
KW - Bone marrow
KW - Fibroblasts
KW - Phage display
KW - Proteasome
KW - Protein modification
UR - http://www.scopus.com/inward/record.url?scp=33744476423&partnerID=8YFLogxK
U2 - 10.1196/annals.1354.068
DO - 10.1196/annals.1354.068
M3 - Journal article
C2 - 16804029
AN - SCOPUS:33744476423
SN - 0077-8923
VL - 1067
SP - 474
EP - 478
JO - Annals of the New York Academy of Sciences
JF - Annals of the New York Academy of Sciences
IS - 1
ER -