Relationship between E1A binding to cellular proteins, c-myc activation and S-phase induction
نویسندگان
چکیده
منابع مشابه
Adenovirus E1A targets p400 to induce the cellular oncoprotein Myc.
Adenovirus E1A drives oncogenesis by targeting key regulatory pathways that are critical for cellular growth control. The interaction of E1A with p400 is essential for many E1A activities, but the downstream target of this interaction is unknown. Here, we present evidence that the oncoprotein transcription factor Myc is the target of this interaction. We show that E1A stabilizes Myc protein via...
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چکیده : این مطالعه تاثیر مدیریت دانش بر رضایتمندی مشتریان با توجه به خدمات الکترونیک در سازمان حمل و نقل و پایانه های استان سیستان و بلوچستان را مورد بررسی قرار می دهد. جامعه آماری این تحقیق مدیران، سرپرستان و کارشناسان مشغول به کار در سازمان حمل و نقل و پایانه های استان سیستان و بلوچستان بوده که مجموعا 94 نفر می باشند. برای تعیین حداقل نمونه از جدول مورگان استفاده شده است. که با توجه به جدول ...
TATA-binding protein and the retinoblastoma gene product bind to overlapping epitopes on c-Myc and adenovirus E1A protein.
Using a protein binding assay, we show that the amino-terminal 204 amino acids of the c-Myc protein interact directly with a key component of the basal transcription factor TFIID, the TATA box-binding protein (TBP). Essentially the same region of the c-Myc protein also binds the product of the retinoblastoma gene, the RB protein. c-Myc protein coimmunoprecipitates with TBP in lysates of mammali...
متن کاملAdenoviral E1A function through Myc.
The study of DNA tumor viruses has been invaluable in uncovering the cellular nodes and pathways that contribute to oncogenesis. Perhaps one of the best-studied oncoproteins encoded by a DNA tumor virus is adenovirus E1A, which modifies the function of key regulatory proteins such as retinoblastoma (Rb) and the chromatin remodeling protein p400. Although the interaction of E1A with Rb has long ...
متن کاملc-Myc Accelerates S-Phase and Requires WRN to Avoid Replication Stress
c-Myc interacts with components of the pre-replication complex and directly regulates DNA replication [1]. However the consequences of this novel c-Myc function on cell cycle dynamics and replication-associated damage are unknown. Here, we show that c-Myc overexpression in primary human fibroblasts markedly accelerates S-phase while c-Myc deficient fibroblasts exhibit a prolonged S-phase. We al...
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ژورنال
عنوان ژورنال: Oncogene
سال: 2006
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1209825