The Extracellular Matrix Protein CCN1 Dictates TNFα and FasL Cytotoxicity In Vivo
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These results show that CCN1 is a physiological regulator of TNF-α- and Fas-mediated apoptosis in vivo.
“These results show that CCN1 is a physiological regulator of TNF-α- and Fas-mediated apoptosis in vivo [111].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [111]
CCN1 significantly enhances the cytotoxicity of TRAIL.
“As described above, CCN1 profoundly alters the activities of inflammatory cytokines such as TNF-α and FasL in vitro and in vivo, and significantly enhances the cytotoxicity of TRAIL [77,111].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [111]
CCN1 alters the activities of inflammatory cytokines such as TNF-α and FasL in vitro and in vivo.
“As described above, CCN1 profoundly alters the activities of inflammatory cytokines such as TNF-α and FasL in vitro and in vivo, and significantly enhances the cytotoxicity of TRAIL [77,111].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [111]
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CCN1/CYR61: the very model of a modern matricellular protein
Lau, L. F. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-011-0778-3 · Cited by 338 · see citing works
Self-citation
- Authors
- Chen, C.-C., Juric, V., & Lau, L. F.
- Affiliations
- University of Illinois Chicago (US)
- University of California, San Francisco (US)
- Corresponding author
- Lau, Lester F.
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer New York
- Published
- 2010-10-22
- Volume
- 691
- Pages
- 595-603
- ISSN
- 0065-2598 (ISSN-L)
- PMC
- PMC3646414
- OpenAlex
- W1485270990
- Cited by
- 8
- References
- 52
- Citations by year
- 2022: 2 · 2021: 1 · 2014: 2 · 2013: 1 · 2012: 1
- FWCI
- 1.17
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL081390, HL81390)
- National Cancer Institute (R01CA046565, CA-46565)
- National Institute of General Medical Sciences (R01GM078492, GM78492)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR061791)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Keywords
- CYR61, CCN family proteins, extracellular matrix, TNF-α, Fas ligand, apoptosis, cytotoxicity, alpha6beta1 integrin, syndecan-4, heparan sulfate proteoglycans, reactive oxygen species, NF-κB signaling, TRAIL, knock-in mice, inflammation
- MeSH terms
- Animals, Extracellular Matrix, Humans, Models, Biological, Tumor Necrosis Factor-alpha, Signal Transduction, Apoptosis, Reactive Oxygen Species, Mice, Fas Ligand Protein, Cysteine-Rich Protein 61
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