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Literature summary for 1.4.3.13 extracted from

  • Choudhary, B.; Zhou, J.; Li, P.; Thomas, S.; Kaartinen, V.; Sucov, H.M.
    Absence of TGFbeta signaling in embryonic vascular smooth muscle leads to reduced lysyl oxidase expression, impaired elastogenesis, and aneurysm (2009), Genesis, 47, 115-121.
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
real-time quantitative PCR enzyme expression analysis in wild-type and mutant mice Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information mutations of the Lox or LoxL1 genes result in a poorly formed vessel wall that is prone to breakdown and aneurysm Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
extracellular
-
Mus musculus
-
-

Organism

Organism UniProt Comment Textmining
Mus musculus
-
genes Lox or LoxL1
-

Source Tissue

Source Tissue Comment Organism Textmining
embryo
-
Mus musculus
-
smooth muscle neural crest- and mesoderm-derived smooth muscle Mus musculus
-

Synonyms

Synonyms Comment Organism
LOX
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Mus musculus
lysyl oxidase
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Mus musculus

Expression

Organism Comment Expression
Mus musculus lineage-specific mutation of the type II TGFbeta receptor gene, Tgfbetar2, in both neural crest- and mesoderm-derived vascular smooth muscle precursors leads to absence of TGFbeta receptor function and reduced lysyl oxidase expression. The result is a poorly organized vascular elastic matrix in late-stage embryos, which is prone to dilation and aneurysm, due to a failure to initiate formation of the elastic matrix, rather than a failure to maintain a preexisting matrix, phenotype of Wnt1Cre/Tgfbr2 mutant embryos, overview down
Mus musculus enzyme expression is induced by TGFbeta treatment in smooth muscle cells up

General Information

General Information Comment Organism
physiological function lysyl oxidases play a critical role in matrix assembly by crosslinking elastin and collagen monomers into fibers Mus musculus