Czech
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
huntington disease/phosphatase
Odkaz je uložen do schránky
Strana 1 z 70 Výsledek
MAP kinase phosphatase 1 (MKP-1/DUSP1) is neuroprotective in Huntington's disease via additive effects of JNK and p38 inhibition.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
We previously demonstrated that sodium butyrate is neuroprotective in Huntington's disease (HD) mice and that this therapeutic effect is associated with increased expression of mitogen-activated protein kinase/dual-specificity phosphatase 1 (MKP-1/DUSP1). Here we show that enhancing MKP-1 expression
Alterations in STriatal-Enriched protein tyrosine Phosphatase expression, activation, and downstream signaling in early and late stages of the YAC128 Huntington's disease mouse model.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Striatal neurodegeneration and synaptic dysfunction in Huntington's disease are mediated by the mutant huntingtin (mHtt) protein. MHtt disrupts calcium homeostasis and facilitates excitotoxicity, in part by altering NMDA receptor (NMDAR) trafficking and function. Pre-symptomatic
Calpain and STriatal-Enriched protein tyrosine phosphatase (STEP) activation contribute to extrasynaptic NMDA receptor localization in a Huntington's disease mouse model.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
In Huntington's disease (HD), the mutant huntingtin (mhtt) protein is associated with striatal dysfunction and degeneration. Excitotoxicity and early synaptic defects are attributed, in part, to altered NMDA receptor (NMDAR) trafficking and function. Deleterious extrasynaptic NMDAR localization and
Striatal-enriched protein tyrosine phosphatase expression and activity in Huntington's disease: a STEP in the resistance to excitotoxicity.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Striatal-enriched protein tyrosine phosphatase (STEP) is highly expressed in striatal projection neurons, the neuronal population most affected in Huntington's disease. Here, we examined STEP expression and phosphorylation, which regulates its activity, in N-terminal exon-1 and full-length mutant
PH domain leucine-rich repeat protein phosphatase 1 contributes to maintain the activation of the PI3K/Akt pro-survival pathway in Huntington's disease striatum.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Dysregulation of gene expression is one of the mechanisms involved in the pathophysiology of Huntington's disease (HD). Here, we examined whether mutant huntingtin regulates the levels of PH domain leucine-rich repeat protein phosphatase 1 (PHLPP1), a phosphatase that specifically dephosphorylates
Changes in nine enzyme markers for neurons, glia, and endothelial cells in agonal state and Huntington's disease caudate nucleus.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Enzymes considered to be markers for neurons (angiotensin converting enzyme, thermolysin-like metalloendopeptidase, alanine aminopeptidase, and glutamate-oxaloacetate transaminase), glia (glutamine synthetase, pyruvate carboxylase, and beta-glucuronidase), and endothelial cells (alkaline phosphatase
Loss of endoplasmic reticulum-associated enzymes in affected brain regions in Huntington's disease and Alzheimer-type dementia.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Post-mortem brain samples from patients with either Huntington's disease, Alzheimer-type dementia or appropriate controls were assayed for endoplasmic reticulum enzymes, NADPH-cytochrome c reductase, neutral alpha-glucosidase, inosine diphosphatase, alpha-mannosidase and glucose-6-phosphatase and
Inhibition of mitochondrial complex II alters striatal expression of genes involved in glutamatergic and dopaminergic signaling: possible implications for Huntington's disease.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Huntington's disease (HD) is a genetic neurodegenerative disorder characterized by motor abnormalities and cognitive impairment. The irreversible succinate dehydrogenase (SD) inhibitor 3-nitropropionic acid (3NP) causes neurodegeration in the striatum resembling HD when administered to rodents or
Regulator of calcineurin (RCAN1-1L) is deficient in Huntington disease and protective against mutant huntingtin toxicity in vitro.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Our work suggests an important new link between the RCAN1 gene and Huntington disease. Huntington disease is caused by expansion of glutamine repeats in the huntingtin protein. How the huntingtin protein with expanded polyglutamines (mutant huntingtin) causes the disease is still unclear, but
Reduced calcineurin protein levels and activity in exon-1 mouse models of Huntington's disease: role in excitotoxicity.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Calcineurin is a serine/threonine phosphatase involved in the regulation of glutamate receptors signaling. Here, we analyzed whether the regulation of calcineurin protein levels and activity modulates the susceptibility of striatal neurons to excitotoxicity in R6/1 and R6/1:BDNF+/- mouse models of
Identification of proteins suppressing the functions of oncogenic phosphatase of regenerating liver 1 and 3.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
The phosphatase of regenerating liver (PRL) family, including PRL-1, PRL-2, and PRL-3, comprises protein tyrosine phosphatases whose deregulation is associated with the tumorigenesis and metastasis of many types of cancer. However, the underlying mechanism is poorly understood. In this study, aiming
Abnormal phosphorylation of synapsin I predicts a neuronal transmission impairment in the R6/2 Huntington's disease transgenic mice.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Motor and cognitive deficits in Huntington's disease (HD) are likely caused by progressive neuronal dysfunction preceding neuronal cell death. Synapsin I is one of the major phosphoproteins regulating neurotransmitter release. We report here an abnormal phosphorylation state of synapsin I in the
Calcineurin inhibitors cause an acceleration of the neurological phenotype in a mouse transgenic for the human Huntington's disease mutation.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Calcineurin (CaN) is a Ca(2+)- and calmodulin-dependent protein serine-threonine phosphatase that is thought to play an important role in the neuronal response to changes in the intracellular Ca(2+) concentration. CaN has been implicated in numerous physiological processes including learning and
PP1 Phosphatase Complexes: Undruggable No Longer.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
The identification of inhibitors targeting regulatory subunits of serine/threonine PP1 phosphatases reported by Krzyzosiak et al. is a significant step in expanding the pharmacological regulation of phosphorylation beyond kinases. The selective inhibitor of the R15B phosphatase regulatory subunit,
Two-track virtual screening approach to identify both competitive and allosteric inhibitors of human small C-terminal domain phosphatase 1.
Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Despite a wealth of persuasive evidence for the involvement of human small C-terminal domain phosphatase 1 (Scp1) in the impairment of neuronal differentiation and in Huntington's disease, small-molecule inhibitors of Scp1 have been rarely reported so far. This study aims to the discovery of both
Nejúplnější databáze léčivých bylin podložená vědou
- Funguje v 55 jazycích
- Bylinné léky podporované vědou
- Rozpoznávání bylin podle obrázku
- Interaktivní mapa GPS - označte byliny na místě (již brzy)
- Přečtěte si vědecké publikace související s vaším hledáním
- Hledejte léčivé byliny podle jejich účinků
- Uspořádejte své zájmy a držte krok s novinkami, klinickými testy a patenty
Zadejte symptom nebo chorobu a přečtěte si o bylinách, které by vám mohly pomoci, napište bylinu a podívejte se na nemoci a příznaky, proti kterým se používá.
* Všechny informace vycházejí z publikovaného vědeckého výzkumu
