Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion - Wikidata - awgldk - TriplyDB

Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion

Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion

http://www.wikidata.org/entity/Q42253318

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Short- and long-term benefits of lenalidomide treatment in patients with lower-risk del(5q) myelodysplastic syndromes PP2A: The Achilles Heal in MDS with 5q Deletion Delayed globin synthesis leads to excess heme and the macrocytic anemia of Diamond Blackfan anemia and del(5q) myelodysplastic syndrome Long-Term Response in a Patient with del(5q) Myelodysplastic Syndrome Who Discontinued Lenalidomide and Obtained a Good Response and Tolerance to Rechallenge.Current therapy of myelodysplastic syndromes Ribosomal proteins and human diseases: pathogenesis, molecular mechanisms, and therapeutic implications Ribosomopathies: mechanisms of disease.Lenalidomide induces lipid raft assembly to enhance erythropoietin receptor signaling in myelodysplastic syndrome progenitors.Clinical utility of lenalidomide in the treatment of myelodysplastic syndromes The relationship of TP53 R72P polymorphism to disease outcome and TP53 mutation in myelodysplastic syndromes Phase 2 study of the lenalidomide and azacitidine combination in patients with higher-risk myelodysplastic syndromes.TP53 and MDM2 single nucleotide polymorphisms influence survival in non-del(5q) myelodysplastic syndromes.Lenalidomide Stabilizes the Erythropoietin Receptor by Inhibiting the E3 Ubiquitin Ligase RNF41.Sequential azacitidine and lenalidomide in patients with high-risk myelodysplastic syndromes and acute myeloid leukaemia: a single-arm, phase 1/2 study.Attenuation of dexamethasone-induced cell death in multiple myeloma is mediated by miR-125b expression TP53 suppression promotes erythropoiesis in del(5q) MDS, suggesting a targeted therapeutic strategy in lenalidomide-resistant patients.Molecular mechanisms of pathology and treatment in Diamond Blackfan Anaemia.Lenalidomide as a disease-modifying agent in patients with del(5q) myelodysplastic syndromes: linking mechanism of action to clinical outcomes Myelodysplastic syndromes with 5q deletion: pathophysiology and role of lenalidomide.p53 and ribosome biogenesis stress: the essentials.Update on the pharmacotherapy for myelodysplastic syndromes.The molecular pathogenesis of the myelodysplastic syndromes.Molecular pathology of myelodysplastic syndromes: new developments and implications for diagnosis and treatment.Recent Advances in the 5q- Syndrome.New Insights into the Pathogenesis of MDS and the rational therapeutic opportunities.A calcium- and calpain-dependent pathway determines the response to lenalidomide in myelodysplastic syndromes UBTD1 induces cellular senescence through an UBTD1-Mdm2/p53 positive feedback loop.Genetics and Epigenetics of Myelodysplastic Syndromes and Response to Drug Therapy: New Insights.RP-MDM2-p53 Pathway: Linking Ribosomal Biogenesis and Tumor Surveillance.Molecular action of lenalidomide in lymphocytes and hematologic malignancies p53-related protein kinase confers poor prognosis and represents a novel therapeutic target in multiple myeloma.FGFR2 mutations in bent bone dysplasia syndrome activate nucleolar stress and perturb cell fate determination.Response to lenalidomide in myelodysplastic syndromes with del(5q): influence of cytogenetics and mutations.The role of p53 in myelodysplastic syndromes and acute myeloid leukemia: molecular aspects and clinical implications.A G polymorphism in the CRBN gene acts as a biomarker of response to treatment with lenalidomide in low/int-1 risk MDS without del(5q).Immunomodulatory Drugs Exert Anti-Leukemia Effects in Acute Myeloid Leukemia by Direct and Immunostimulatory Activities.Genetic susceptibility to thalidomide embryopathy in humans: Study of candidate development genes deletion in luminal cells of mature prostate induces replication stress and senescence in vivo

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Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion

http://www.wikidata.org/entity/Q42253318

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name

Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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Lenalidomide promotes p53 degr ...... me with chromosome 5q deletion

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D Billingsley

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D Sallman

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G Caceres

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P2860

Mdm2 is a RING finger-dependent ubiquitin protein ligase for itself and p53

p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53

Identification of a primary target of thalidomide teratogenicity

Identification of RPS14 as a 5q- syndrome gene by RNA interference screen

Phosphorylation on Thr-55 by TAF1 mediates degradation of p53: a role for TAF1 in cell G1 progression

Regulation of the MDM2-p53 pathway by ribosomal protein L11 involves a post-ubiquitination mechanism

The DNA damage response: putting checkpoints in perspective

Activity of MDM2, a ubiquitin ligase, toward p53 or itself is dependent on the RING finger domain of the ligase

Regulation of HDM2 activity by the ribosomal protein L11

Posttranslational modification of MDM2

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10.1038/ONC.2012.139

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Erika A. Eksioglu

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1005348672

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22525275

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protein ubiquitination

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3751397

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