The role of human kallikrein 6,
clusterin and adiponectin as potential blood biomarkers of dementia.
Another AD risk gene is
clusterin (CLU) known as apolipoprotein J (APOJ) (14), and it directly binds A[beta] and regulates the A[beta] pathology (15).
The tumor cells consistently express vimentin, with variable positivity for D2-40, CD34, CD68, smooth muscle actin, keratin, and p53, but lack other mesenchymal, epithelial markers, such as S100 protein, desmin, neuron-specific enolase, epithelial membrane antigen, HMB-45,
clusterin, and leukocyte markers (CD15, CD30, CD45).
In AD, amyloid precursor protein (APP) and presenilin (PS) are already the definitive virulence genes.[1] For SAD >90% of AD, major influencing genes include apolipoprotein E (ApoE) gene,
clusterin gene, complement receptor 1 gene, and phospholipids bind to clathrin protein (PICALM) gene.[2] Along with the development of genetic research into AD, more new genetic loci for AD have been discovered, including cholesterol metabolism gene (CH25H, ABCAL, and CH24H),[3] Sterol O-acyltransferase (Soat1) and prostaglandin-endoperoxide synthase 2 (Ptgs2)[4] genes, and angiotensin-converting enzyme gene [5] are some of these.
Localization of proliferating cell nuclear antigen, vimentin, c-Fos, and
clusterin in the postischemic kidney.
Salminen, "Valproic acid stimulates
clusterin expression in human astrocytes: implications for Alzheimer's disease," Neuroscience Letters, vol.
Mattsson et al., "Complement and
clusterin in the spinal cord dorsal horn and gracile nucleus following sciatic nerve injury in the adult rat," Neuroscience, vol.
Clusterin (CLU) is a stress-induced chaperone involved in neuronal protection [38].
The tumor cells were also negative for HMB-45, CD15, CD20, CD21, CD23, CD43, CD45, desmin, myogenin, calretinin, myeloperoxidase, D2-40, CD68, and
clusterin (Figure 1(e)).