Literature summary for 3.4.24.82 extracted from

Rao, N.; Ke, Z.; Liu, H.; Ho, C.; Kumar, S.; Xiang, W.; Zhu, Y.; Ge, R.
ADAMTS4 and its proteolytic fragments differentially affect melanoma growth and angiogenesis in mice (2013), Int. J. Cancer, 133, 294-306.

Search for more literature for 3.4.24.82

Application

Application	Comment	Organism
medicine	full-length ADAMTS4 and its catalytically more active N-terminal 53 kDa autocatalytic fragment both promote B16 melanoma growth and angiogenesis in mice. Overexpression of its catalytically inactive E362A mutant or truncated fragments containing only the C-terminal ancillary domains suppresses melanoma growth and angiogenesis under similar conditions. The single thrombospondin-type 1 repeat domain is essential and sufficient for the antitumorigenic activity of the catalytically inactive ADAMTS4 isoforms. Suppression of tumor growth and angiogenesis in mice is accompanied by a significant increase in tumor cell apoptosis, whereas tumor cell proliferation is not affected	Mus musculus

Protein Variants

Protein Variants	Comment	Organism
E362A	catalytically inactive	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q8BNJ2	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

General Information

General Information	Comment	Organism
physiological function	full-length ADAMTS4 and its catalytically more active N-terminal 53 kDa autocatalytic fragment both promote B16 melanoma growth and angiogenesis in mice. Overexpression of its catalytically inactive E362A mutant or truncated fragments containing only the C-terminal ancillary domains suppresses melanoma growth and angiogenesis under similar conditions. The single thrombospondin-type 1 repeat domain is essential and sufficient for the antitumorigenic activity of the catalytically inactive ADAMTS4 isoforms. Suppression of tumor growth and angiogenesis in mice is accompanied by a significant increase in tumor cell apoptosis, whereas tumor cell proliferation is not affected	Mus musculus

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)