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telangiectasis/phosphatase
Link salvestatakse lõikelauale
Leht 1 alates 159 tulemused
Utilizing protein phosphatase inhibitors to define PP2A as a regulator of ataxia-telangiectasia mutated.
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Ataxia-telangiectasia mutated (ATM) is a serine/threonine protein kinase that plays a central role in controlling the cellular response to DNA double-strand breaks caused by ionizing radiation. Ionizing radiation induces the autophosphorylation of ATM on serine 1981; however, the precise mechanisms
Mice lacking protein phosphatase 5 are defective in ataxia telangiectasia mutated (ATM)-mediated cell cycle arrest.
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Protein phosphatase 5 (Ppp5), a tetratricopeptide repeat domain protein, has been implicated in multiple cellular functions, including cellular proliferation, migration, differentiation and survival, and cell cycle checkpoint regulation via the ataxia telangiectasia mutated/ATM and Rad3-related
Autophosphorylation of ataxia-telangiectasia mutated is regulated by protein phosphatase 2A.
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Ionizing radiation induces autophosphorylation of the ataxia-telangiectasia mutated (ATM) protein kinase on serine 1981; however, the precise mechanisms that regulate ATM activation are not fully understood. Here, we show that the protein phosphatase inhibitor okadaic acid (OA) induces
Phosphorylation of polynucleotide kinase/ phosphatase by DNA-dependent protein kinase and ataxia-telangiectasia mutated regulates its association with sites of DNA damage.
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Human polynucleotide kinase/phosphatase (PNKP) is a dual specificity 5'-DNA kinase/3'-DNA phosphatase, with roles in base excision repair, DNA single-strand break repair and non-homologous end joining (NHEJ); yet precisely how PNKP functions in the repair of DNA double strand breaks (DSBs) remains
PTEN (Phosphatase and Tensin Homolog) Connection in Hereditary Hemorrhagic Telangiectasia 2.
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Role of wild-type p53-induced phosphatase 1 in cancer.
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Wild-type p53-induced phosphatase (Wip1) is a member of the protein phosphatase type 2C family and is an established oncogene due to its dephosphorylation of several tumor suppressors and negative control of the DNA damage response system. It has been reported to dephosphorylate p53, ataxia
A novel ATM-dependent pathway regulates protein phosphatase 1 in response to DNA damage.
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Protein phosphatase 1 (PP1), a major protein phosphatase important for a variety of cellular responses, is activated in response to ionizing irradiation (IR)-induced DNA damage. Here, we report that IR induces the rapid dissociation of PP1 from its regulatory subunit inhibitor-2 (I-2) and that the
Linear growth and endocrine function in children with ataxia telangiectasia.
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BACKGROUND
Ataxia telangiectasia (AT) is a rare, genetic, primary immune deficiency disease characterized by immunodeficiency and neurological manifestations, with an increased tendency to infection, malignancy, and autoimmune diseases. Both growth delay and endocrine abnormalities are occasionally
Clinical Outcomes of Patients with Severe Hepatic Hereditary Hemorrhagic Telangiectasia After Banding of the Hepatic Artery and Banding/Ligation of Branches of the Hepatic Artery.
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OBJECTIVE
To evaluate the effectiveness of double banding/ligation of hepatic arteries in treating patients with hepatic hereditary hemorrhagic telangiectasia (HHHT).
METHODS
From January 2004 to December 2013, 35 patients were diagnosed with HHHT, among whom 11 woman and two men with a mean ± SD
P65-mediated miR-590 inhibition modulates the chemoresistance of osteosarcoma to doxorubicin through targeting wild-type p53-induced phosphatase 1.
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Osteosarcoma (OS) is a primary malignant bone tumor with high morbidity. Developing new therapeutic approaches with neoadjuvant is of great interest in OS treatment. Reportedly, ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and radiation resistance gene 3 related (ATR)-p53 signaling is
The oncogenic phosphatase PPM1D confers cisplatin resistance in ovarian carcinoma cells by attenuating checkpoint kinase 1 and p53 activation.
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Cisplatin (CDDP: cis-diamminedichloroplatinum) resistance is a major hurdle in the treatment of human ovarian cancer (OVCA). A better understanding of the mechanisms of CDDP resistance can greatly improve therapeutic outcome for patients. A determinant of CDDP sensitivity in OVCA, p53, is activated
A human homologue of the checkpoint kinase Cds1 directly inhibits Cdc25 phosphatase.
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BACKGROUND
In human cells, the mitosis-inducing kinase Cdc2 is inhibited by phosphorylation on Thr14 and Tyr15. Disruption of these phosphorylation sites abrogates checkpoint-mediated regulation of Cdc2 and renders cells highly sensitive to agents that damage DNA. Phosphorylation of these sites is
Hereditary acrolabial telangiectasia. A report of familial blue lips, nails, and nipples.
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We describe a mother and two daughters who had the following clinical manifestations: bluish discoloration of the vermillion ridge of the lips, nipple areolae, and nail beds; discrete telangiectasia of the chest, elbows, and dorsa of the hands; varicosities of the lower part of the legs; and (in the
Phosphorylation of Chk1 by ATR is antagonized by a Chk1-regulated protein phosphatase 2A circuit.
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Logi sisse
In higher eukaryotic organisms, the checkpoint kinase 1 (Chk1) contributes essential functions to both cell cycle and checkpoint control. Chk1 executes these functions, in part, by targeting the Cdc25A protein phosphatase for ubiquitin-mediated proteolysis. In response to genotoxic stress, Chk1 is
Regulation of BRCA1 phosphorylation by interaction with protein phosphatase 1alpha.
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Logi sisse
Numerous reports have revealed that the tumor suppressor BRCA1 may play an important role in DNA damage repair. BRCA1 is expressed and phosphorylated during cell cycle progression and after DNA damage. BRCA1 is hypophosphorylated in G0-G1 and probably during mitosis as well. Kinases known to
Kõige täiuslikum ravimtaimede andmebaas, mida toetab teadus
- Töötab 55 keeles
- Taimsed ravimid, mida toetab teadus
- Maitsetaimede äratundmine pildi järgi
- Interaktiivne GPS-kaart - märgistage ürdid asukohas (varsti)
- Lugege oma otsinguga seotud teaduspublikatsioone
- Otsige ravimtaimi nende mõju järgi
- Korraldage oma huvisid ja hoidke end kursis uudisteuuringute, kliiniliste uuringute ja patentidega
Sisestage sümptom või haigus ja lugege ravimtaimede kohta, mis võivad aidata, tippige ürdi ja vaadake haigusi ja sümptomeid, mille vastu seda kasutatakse.
* Kogu teave põhineb avaldatud teaduslikel uuringutel
