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Gene Review:

CLU - clusterin

Canis lupus familiaris

Tsuchiya, Y. et al., Gutacker, C. et al., Martín-Belmonte, F. et al., Losch, A. et al., Lösch, A. et al., et al.

Tsuchiya, Tominaga, Matsubayashi, Jindo, Furuhama, Suzuki,

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High impact information on CLU

Furthermore, the overproduction of VIP36 greatly stimulated the secretion of a major apical secretory glycoprotein of MDCK cells, clusterin, which was found to carry at least one high mannose-type glycan and to be recognized by VIP36 [1].
Apical secretion of gp80/clusterin was also inhibited by elimination of endogenous MAL [2].
Addition of dithiothreitol (DTT) to the culture medium of Madin-Darby canine kidney (MDCK) cells blocks transport of newly synthesized gp80 (clusterin, apolipoprotein J), a soluble marker protein for apical exocytosis in this epithelial cell line [3].
Multiple signal transduction pathways regulate clusterin (gp 80) gene expression in MDCK cells [4].
Clusterin (gp 80, apolipoprotein J, TRPM-2) is a widely expressed multifunctional glycoprotein [4].

Biological context of CLU

Treatment with epidermal growth factor also represses clusterin gene expression in MDCK cells [4].
These results demonstrate that changes in renal clusterin mRNA may reflect the progression or severity of RPN, whereas upregulation of tissue kallikrein mRNA may subsequently play a compensating role in the prevention of RPN [5].

Anatomical context of CLU

To examine the transport of the single subunits of the glycoprotein complex gp80 (clusterin, apolipoprotein J), a marker protein for apical exocytosis and main secretory product of Madin-Darby canine kidney (MDCK) cells, several mutant cDNAs were constructed and expressed in the fibroblastic baby hamster kidney (BHK-21) cell line [6].

Associations of CLU with chemical compounds

We have examined the secretion of recombinant Tg and gp80/clusterin, a major endogenous secretory protein not detected in Triton X-100 insoluble rafts, for the investigation of the involvement of MAL in the constitutive apical secretory pathway of MDCK cells [2].
We show here that, in the kidney-derived epithelial cell line MDCK, clusterin mRNA is repressed by glucocorticoids and by progesterone [4].

Analytical, diagnostic and therapeutic context of CLU

Molecular cloning, characterization and expression of a novel retinal clusterin-like protein cDNA [7].
By quantitative real-time RT-PCR analysis with renal morphological aspects, individual findings showed that renal clusterin mRNA was increased in dogs with severe renal injury, and renal tissue kallikrein also increased, presumably related to hemodynamics [5].

References

Involvement of VIP36 in intracellular transport and secretion of glycoproteins in polarized Madin-Darby canine kidney (MDCK) cells. Hara-Kuge, S., Ohkura, T., Ideo, H., Shimada, O., Atsumi, S., Yamashita, K. J. Biol. Chem. (2002) [Pubmed]
MAL mediates apical transport of secretory proteins in polarized epithelial Madin-Darby canine kidney cells. Martín-Belmonte, F., Arvan, P., Alonso, M.A. J. Biol. Chem. (2001) [Pubmed]
Dithiothreitol treatment of Madin-Darby canine kidney cells reversibly blocks export from the endoplasmic reticulum but does not affect vectorial targeting of secretory proteins. Lösch, A., Koch-Brandt, C. J. Biol. Chem. (1995) [Pubmed]
Multiple signal transduction pathways regulate clusterin (gp 80) gene expression in MDCK cells. Gutacker, C., Flach, R., Diel, P., Klock, G., Koch-Brandt, C. J. Mol. Endocrinol. (1996) [Pubmed]
Investigation on urinary proteins and renal mRNA expression in canine renal papillary necrosis induced by nefiracetam. Tsuchiya, Y., Tominaga, Y., Matsubayashi, K., Jindo, T., Furuhama, K., Suzuki, K.T. Arch. Toxicol. (2005) [Pubmed]
Oligomerization supports transport of a mutant secretory protein out of the endoplasmic reticulum. Losch, A., Henkel, K., Wagner, M., Urban, J., Koch-Brandt, C. Eur. J. Cell Biol. (1996) [Pubmed]
Molecular cloning, characterization and expression of a novel retinal clusterin-like protein cDNA. Zhang, Q., Ray, K., Acland, G.M., Czarnecki, J.M., Aguirre, G.D. Gene (2000) [Pubmed]

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