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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Anthrax toxin receptor 1

TEM8, anthrax toxin receptor, tumor endothelial marker 8, ANTXR1, anthrax toxin receptor 1
This gene encodes a type I transmembrane protein and is a tumor-specific endothelial marker that has been implicated in colorectal cancer. The encoded protein has been shown to also be a docking protein or receptor for Bacillus anthracis toxin, the causative agent of the disease, anthrax. The binding of the protective antigen (PA) component, of the tripartite anthrax toxin, to this receptor protein mediates delivery of toxin components to the cytosol of cells. Once inside the cell, the other two components of anthrax toxin, edema factor (EF) and lethal factor (LF) disrupt normal cellular processes. Three alternatively spliced variants that encode different protein isoforms have been described. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: JHF, CAN, HAD, V1a, ACID
Papers on TEM8
A complex role of anthrax toxin receptor 2 polymorphisms and capillary morphogenesis protein 2 in ankylosing spondylitis pathogenesis.
Sun et al., Beijing, China. In Clin Rheumatol, Feb 2016
UNASSIGNED: This study investigated the role of anthrax toxin receptor 2 (ANTXR2) gene polymorphisms and capillary morphogenesis protein 2 (CMG2) expression in susceptibility and pathogenesis to ankylosing spondylitis (AS) in the Han Chinese in Beijing.
Anthrax Toxin Receptor 1 Is Essential for Arteriogenesis in a Mouse Model of Hindlimb Ischemia.
Duesbery et al., Grand Rapids, United States. In Plos One, Dec 2015
Anthrax toxin receptor 1/tumor endothelial marker 8 (Antxr1 or TEM8) is up-regulated in tumor vasculature and serves as a receptor for anthrax toxin, but its physiologic function is unclear.
Infantile systemic hyalinosis in identical twins.
Venugopal et al., Hyderābād, India. In Intractable Rare Dis Res, Nov 2015
It is a rare, progressive, fatal autosomal recessive condition characterized by widespread deposition of hyaline material in many tissues caused by mutations in the anthrax toxin receptor 2 gene - ANTXR2.
EpCAM-Independent Enrichment of Circulating Tumor Cells in Metastatic Breast Cancer.
Disseminated Cancer Cell Network (DCC Net) Duesseldorf et al., Düsseldorf, Germany. In Plos One, 2014
The expression of respective proteins (Trop2, CD49f, c-Met, CK8, CD44, ADAM8, CD146, TEM8, CD47) was verified by immunofluorescence on EpCAMpos (e.g.
Anthrax Susceptibility: Human Genetic Polymorphisms Modulating ANTXR2 Expression.
Chen et al., Beijing, China. In Toxins (basel), 2014
Anthrax toxin causes anthrax pathogenesis and expression levels of ANTXR2 (anthrax toxin receptor 2) are strongly correlated with anthrax toxin susceptibility.
Molecular determinants for a cardiovascular collapse in anthrax.
Goldman et al., Ben Mehidi, Algeria. In Front Biosci (elite Ed), 2013
A recent study using mice that either lacked the anthrax toxin receptor in specific cells and corresponding mice expressing the receptor in specific cell types demonstrated that cardiovascular cells are critical for disease mediated by anthrax lethal toxin.
Key tissue targets responsible for anthrax-toxin-induced lethality.
Leppla et al., Bethesda, United States. In Nature, 2013
Here we generated cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2 (CMG2)-null mice and cell-type-specific CMG2-expressing mice and challenged them with the toxins.
Anthrax toxin receptor 2a controls mitotic spindle positioning.
González-Gaitán et al., Genève, Switzerland. In Nat Cell Biol, 2013
Here we show that, in dorsal epiblast cells, anthrax toxin receptor 2a (Antxr2a) accumulates in a polarized cortical cap, which is aligned with the embryonic A-V axis and forecasts the division plane.
Binding of filamentous actin to anthrax toxin receptor 1 decreases its association with protective antigen.
Mogridge et al., Toronto, Canada. In Biochemistry, 2012
An acidic region in the cytosolic tail of ANTXR1 decreases actin association, sending a signal that prevents binding of ANTXR1 to the protective antigen and providing evidence that cytoskeletal dynamics regulate ANTXR1 function.
TEM8/ANTXR1 blockade inhibits pathological angiogenesis and potentiates tumoricidal responses against multiple cancer types.
St Croix et al., Frederick, United States. In Cancer Cell, 2012
Disruption of Tem8 results in impaired growth of human tumor xenografts of diverse origin including melanoma, breast, colon, and lung cancer.
Tumor endothelial marker 8 overexpression in breast cancer cells enhances tumor growth and metastasis.
Bathe et al., Calgary, Canada. In Cancer Invest, 2011
TEM8.1 expression in breast cancer cells confers a more aggressive, proangiogenic phenotype.
Tumor endothelial marker 8 expression in triple-negative breast cancer.
Grobmyer et al., Gainesville, United States. In Anticancer Res, 2011
TEM8 was expressed at a higher level in the stroma adjacent to the triple-negative breast cancer in all cases, with focal immunoreactive areas within the tumor.
[Bacillus anthracis: a molecular look at a famous pathogen].
Cataldi et al., Saudi Arabia. In Rev Argent Microbiol, 2011
Finally, the two anthrax toxin protective antigen receptors, ANTXR1/TEM8 and ANTXR2/CMG2, essential for the interaction of the pathogen with the host, are presented.
Tumor endothelial marker 8 amplifies canonical Wnt signaling in blood vessels.
Werner et al., Atlanta, United States. In Plos One, 2010
postulate that the developmentally controlled expression of TEM8 modulates endothelial cell response to canonical Wnt signaling to regulate vessel patterning and density
Targeting the anthrax receptors, TEM-8 and CMG-2, for anti-angiogenic therapy.
Rogers et al., Boston, United States. In Front Biosci, 2010
The anthrax toxin receptors tumor endothelial marker-8 (TEM-8) and capillary morphogenesis gene-2 (CMG-2) are responsible for allowing entry of anthrax toxin into host cells.
Receptors of anthrax toxin and cell entry.
Young et al., Lausanne, Switzerland. In Mol Aspects Med, 2009
This review summarizes what is known about the molecular details of the protective antigen (PA) toxin subunit interaction with either the ANTXR1 and ANTXR2 cellular receptors, and how receptor-type can dictate the low pH threshold of PA pore formation.
Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma.
Olsen et al., Boston, United States. In Nat Med, 2008
Low VEGFR1 expression in hemECs is caused by reduced activity of a pathway involving beta1 integrin, the integrin-like receptor tumor endothelial marker-8 (TEM8), VEGFR2 and NFAT.
LRP6 holds the key to the entry of anthrax toxin.
Hultgren et al., Wichita, United States. In Cell, 2006
LRP6 acts as a coreceptor with either TEM8 or CMG2, the two previously identified receptors for anthrax toxin.
The LDL receptor-related protein LRP6 mediates internalization and lethality of anthrax toxin.
Cohen et al., Stanford, United States. In Cell, 2006
Fluorescence microscopy and biochemical analyses showed that LRP6 enables toxin internalization by interacting at the cell surface with PA receptors TEM8/ATR and/or CMG2 to form a multicomponent complex that enters cells upon PA binding.
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