Allosteric inhibition of lysyl oxidase–like-2 impedes the development of a pathologic microenvironment

By Vivian Barry-Hamilton, Rhyannon Spangler, Derek Marshall, S. McCauley, Hector M Rodriguez, M. Oyasu, Amanda J Mikels, Maria Vaysberg, Haben Ghermazien, C. Wai and 13 more. Nature Medicine, 2010

820 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/4df62ab6cfcd03b871424a33305da9f11432af75

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

In Molecular Biology

Citations in the corpus

Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy (2020, background): “Lysyl oxidases are also significantly upregulated in many tumors, especially in desmoplastic cancers (Peyrol et al., 1997; Erler et al., 2006; Barry-Hamilton et al., 2010).”
Extracellular matrix structure. (2016, background): “Inhibition of LOX activity by using specific inhibitors such AB0023 may prevent ECM stiffening and thus facilitate the penetration of administrated drugs [361].”
Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Potent anti-fibrotic activity in bleomycin based mouse model of liver fibrosis via inhibition of collagen-crosslinking and its downstream activating effect on TGF-β1 signaling that contributes to myofibroblast simulation [328].”
Cellular and molecular mechanisms in kidney fibrosis. (2014, neutral): “bition of the crosslinking enzyme lysyloxidase-2 markedly inhibits both fibrogenesis and collagen crosslinking without affecting normal matrix turnover in other organs (97).”
Remodeling and homeostasis of the extracellular matrix: implications for fibrotic diseases and cancer (2011, neutral): “…in situ cross-linking of native ECM components (Butcher et al., 2009) either enzymatically, using LOX (Erler et al., 2009) and LOX family proteins (Barry-Hamilton et al., 2010), or through non-enzymatic reactions such as glycation using ribose or glucose (Paszek et al., 2005; Erler et al., 2006;…”
The extracellular matrix modulates the hallmarks of cancer (2014, positive): “Thus, abrogation of ECM remodeling or deposition into the stroma of tumors in preclinical models of cancer progression has successfully retarded cancer progression [125 – 128].”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “Furthermore, antibody-mediated inhibition of the enzyme LOX-like 2 (LOXL2) suppresses fibrosis and its progression in a variety of organ systems, including tumor desmoplasia.(69) However, it remains unclear whether this effect is due to reduced ECM stiffness.”
Hepatic fibrosis: Concept to treatment. (2015, background): “An important advance has been the identification of lysyl oxidase 2 (LOXL2) in catalyzing the cross-linking of extracellular collagens [25].”
Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments (2023, background): “Several research has proved that BANP treatment can suppress proliferation and invasion of tumor cells [395, 566, 567].”
The myofibroblast matrix: implications for tissue repair and fibrosis (2013, neutral): “LOXL2-mediated matrix remodeling in metastasis and mammary gland involution.”
Mechanisms of fibrosis: therapeutic translation for fibrotic disease (2012, neutral): “A humanized monoclonal antibody targeting lysyl oxidase–like-2, an enzyme that catalyzes the cross-linking of collagen, is being explored by Gilead Sciences as a treatment for cardiac fibrosis, IPF and liver fibrosis 163 .”