Olink

Olink®
Part of Thermo Fisher Scientific

Explore HT

Gene
CLU

Uniprot
P10909

Protein
Clusterin

See alternative names Aging-associated gene 4 protein,
Apolipoprotein J,
Complement cytolysis inhibitor,
Complement-associated protein SP-40,40,
Complement cytolysis inhibitor b chain,
ApoJbeta,
Complement cytolysis inhibitor a chain,
ApoJalpha,
Testosterone-repressed prostate message 2,
Sulfated glycoprotein 2,
NA1/NA2,
Ku70-binding protein 1

Uniprot Function Description

Does not affect caspase or BAX-mediated intrinsic apoptosis and TNF-induced NF-kappa-B-activity.

Does not affect caspase or BAX-mediated intrinsic apoptosis and TNF-induced NF-kappa-B-activity (PubMed:24073260). Promotes cell death through interaction with BCL2L1 that releases and activates BAX (PubMed:21567405).

Functions as extracellular chaperone that prevents aggregation of non native proteins (PubMed:11123922, PubMed:19535339). Prevents stress-induced aggregation of blood plasma proteins (PubMed:11123922, PubMed:12176985, PubMed:17260971, PubMed:19996109). Inhibits formation of amyloid fibrils by APP, APOC2, B2M, CALCA, CSN3, SNCA and aggregation-prone LYZ variants (in vitro) (PubMed:12047389, PubMed:17412999, PubMed:17407782). Does not require ATP (PubMed:11123922). Maintains partially unfolded proteins in a state appropriate for subsequent refolding by other chaperones, such as HSPA8/HSC70 (PubMed:11123922). Does not refold proteins by itself (PubMed:11123922). Binding to cell surface receptors triggers internalization of the chaperone-client complex and subsequent lysosomal or proteasomal degradation (PubMed:21505792). Protects cells against apoptosis and against cytolysis by complement (PubMed:2780565). Intracellular forms interact with ubiquitin and SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complexes and promote the ubiquitination and subsequent proteasomal degradation of target proteins (PubMed:20068069). Promotes proteasomal degradation of COMMD1 and IKBKB (PubMed:20068069). Modulates NF-kappa-B transcriptional activity (PubMed:12882985). A mitochondrial form suppresses BAX-dependent release of cytochrome c into the cytoplasm and inhibit apoptosis (PubMed:16113678, PubMed:17689225). Plays a role in the regulation of cell proliferation (PubMed:19137541). An intracellular form suppresses stress-induced apoptosis by stabilizing mitochondrial membrane integrity through interaction with HSPA5 (PubMed:22689054). Secreted form does not affect caspase or BAX-mediated intrinsic apoptosis and TNF-induced NF-kappa-B-activity (PubMed:24073260). Secreted form act as an important modulator during neuronal differentiation through interaction with STMN3 (By similarity). Plays a role in the clearance of immune complexes that arise during cell injury (By similarity).

Sample type

Recommended sample types are human plasma and serum. For other sample types e.g cerebrospinal fluid, (CSF), tissue or cell lysate, please contact support@olink.com for more information. Please note that protein expression levels are expected to vary in different sample types and certain assays may be affected by interfering substances such as hemolysate.

Precision

Precision (repeatability) is calculated from linearized NPX values over LOD.

Within run precision Coefficient of Variation (CV)
12%

Analytical measuring range

The technical data reported below refers to the measured value in the in vitro validation assays run using known concentrations of recombinant antigen.

LOD (NPX)
-1.1
Hooked
Yes
Hook (NPX)
4.9

Dilution factor

For optimal assay readout, Olink assays are run using different dilutions of the original samples e.g. undiluted, 1:10, or higher. The dilution factor for this assay is noted below and should be taken into account when estimating the appropriate addressable biological concentration of the protein based on the in vitro validation data.

Dilution factor
1:100000

Biomarker Validation Data

Additional validation data, as well as a more detailed description of how the Olink panels are quality controlled can be found in our Data Validation documents – go to Document download center

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