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telangiectasis/protease
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Seite 1 von 36 Ergebnisse
An ataxia telangiectasia model: inefficient cell differentiation and possible reversal by serine protease inhibitors, tumor necrosis factor inhibitors, dexamethasone, and glutathione enhancers.
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Ataxia telangiectasia (AT) is a rare genetic disorder. Symptoms of the disease include cerebellar ataxia, depressed immunoresponsiveness, increased sensitivity to radiation, and leukemias. Various kinds of AT cells show reduced efficiency of differentiation. The ataxia telangiectasia gene (ATM) may
Evidence for the existence of an actin-derived protein in ataxia-telangiectasia lymphoblastoid cell lines.
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In a number of lymphoblastoid cell lines from individuals with the genetic disease ataxia-telangiectasia (A-T), a decrease in the levels of actin and a concomitant increase in the levels of a protein species of 37K has been observed to occur following high cell density. In this paper we describe
1H, 15N, and 13C chemical shift assignments of the micelle immersed FAT C-terminal (FATC) domains of the human protein kinases ataxia-telangiectasia mutated (ATM) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) fused to the B1 domain of streptococcal protein G (GB1).
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FAT C-terminal (FATC) is a circa 33 residue-long domain. It controls the kinase functionality in phosphatidylinositol-3 kinase-related kinases (PIKKs). Recent NMR- and CD-monitored interaction studies indicated that the FATC domains of all PIKKs can interact with membrane mimetics albeit with
Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea.
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Acne rosacea is an inflammatory skin disease that affects 3% of the US population over 30 years of age and is characterized by erythema, papulopustules and telangiectasia. The etiology of this disorder is unknown, although symptoms are exacerbated by factors that trigger innate immune responses,
NF-κB induction of the SUMO protease SENP2: A negative feedback loop to attenuate cell survival response to genotoxic stress.
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Activation of NF-κB, pivotal for immunity and oncogenesis, is tightly controlled by multiple feedback mechanisms. In response to DNA damage, SUMOylation of NEMO (NF-κB essential modulator) is critical for NF-κB activation; however, the SUMO proteases and feedback mechanisms involved remain unknown.
Inhibition of ataxia telangiectasia-p53-E2F-1 pathway in neurons as a target for the prevention of neuronal apoptosis.
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Over the last few decades, understanding of the mechanisms involved in the process of neuronal cell death has grown. Recent findings have established that DNA damage, and specifically ataxia telangiectasia mutated protein (ATM), is key to the cascade of regulation of neuronal apoptosis. Another
Cleavage of ATM during radiation-induced apoptosis: caspase-3-like apoptotic protease as a candidate.
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OBJECTIVE
To study the relationship of ionizing radiation-induced apoptosis with the integrity of ATM (mutated in ataxia telangiectasia) that has a critical role in DNA damage sensing and repair, cell-cycle checkpoint controls and maintenance of genomic stability.
METHODS
U937 cells were treated
[Physiopathology of rosacea. Redness, telangiectasia, and rosacea].
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The physiopathology of rosacea involves a large number of factors that are at times difficult to correlate. There is not a single physiopathological model. Nevertheless, today it seems to have been established that two essential factors are involved: vascular and inflammatory. The disease occurs in
Pathophysiology of rosacea: redness, telangiectasia, and rosacea.
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The pathophysiology of rosacea involves a large number of factors that are at times difficult to correlate. There is not a single physiopathological model. Nevertheless, today it seems to have been established that two essential factors are involved: vascular and inflammatory. The disease occurs in
Tyrosyl-DNA Phosphodiesterase I a critical survival factor for neuronal development and homeostasis.
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Tyrosyl-DNA phosphodiesterase I (TDP1), like most DNA repair associated proteins, is not essential for cell viability. However, dysfunctioning TDP1 or ATM (ataxia telangiectasia mutated) results in autosomal recessive neuropathology with similar phenotypes, including cerebellar atrophy. Dual
Antiapoptotic effects of roscovitine on camptothecin-induced DNA damage in neuroblastoma cells.
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In the present study dopaminergic neuroblastoma B65 cells were exposed to Camptothecin (CPT) (0.5-10 μM), either alone or in the presence of roscovitine (ROSC). The results show that CPT induces apoptosis through the activation of ataxia telangiectasia mutated (ATM)-induced cell-cycle alteration in
Real-World Efficacy of Azelaic Acid 15% Gel for the Reduction of Inflammatory Lesions of Rosacea.
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Approximately 16 million Americans have rosacea, an inflammatory cutaneous disorder with central facial erythema, papules, pustules, telangiectasia, flushing, and swelling being among the more commonly recognized features. Overexpression of cathelicidin peptide LL-37 has been implicated in the
Cleavage and inactivation of ATM during apoptosis.
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The activation of the cysteine proteases with aspartate specificity, termed caspases, is of fundamental importance for the execution of programmed cell death. These proteases are highly specific in their action and activate or inhibit a variety of key protein molecules in the cell. Here, we study
Hepatitis C virus infection downregulates the ligands of the activating receptor NKG2D.
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Natural killer (NK) cells are a major component of the host innate immune defense against various pathogens. Several viruses, including hepatitis C virus (HCV), have developed strategies to evade the NK-cell response. In our study, we found HCV infection could trigger DNA damage response by both
Isolation of an X-ray-responsive element in the promoter region of tissue-type plasminogen activator: potential uses of X-ray-responsive elements for gene therapy.
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Tissue-type plasminogen activator (t-PA) was induced over 50-fold after X irradiation in radioresistant human melanoma cells (Boothman et al., Cancer Res. 51, 5587-5595, 1991). Activities of t-PA were induced 14-fold in ataxia telangiectasia, 9-fold in Bloom's syndrome and 6-fold in Fanconi's anemia
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