Rb cov proteins tuaj yeem ua phosphorylated ob qho tib si ntawm A / B domains ntawm lub hnab tshos cheeb tsam thiab ntawm C-terminal domain. Lub ntsiab hypothesis yog tias cov phosphorylation ntawm carboxy terminus ntawm pRb los ntawm cyclin D / cdk4 (los yog ckd6) ua rau muaj kev hloov pauv hloov, uas hloov HDAC khi rau pRb los ntawm nws LXCXE motif.
Puas yog retinoblastoma nquag thaum phosphorylated?
Cov retinoblastoma protein (RB1) yog ib qho tseem ceeb ntawm cov qog nqaij hlav qog uas thaiv cov kab mob ntawm tes los ntawm inhibiting E2F transcription yam tseem ceeb thaum unphosphorylated. Ntawm phosphorylation los ntawm cyclin-dependent kinases, RB1 yog tsom rau kev degradation thiab E2F cov ntsiab lus tau tso cai ua haujlwm
Puas Rb phosphorylate?
Tus Retinoblastoma (Rb) qog suppressor protein is tswj los ntawm phosphorylation thiab ua lub luag haujlwm hauv ntau cov txheej txheem ntawm tes tseem ceeb xws li kev loj hlob, kev sib txawv, kev loj hlob thiab apoptosis.
Yuav ua li cas cuam tshuam los thaiv Rb phosphorylation?
Peb cov txiaj ntsig tau qhia tias kev tawm tsam ntawm Rb phosphorylation los ntawm inhibition ntawm CDK4 / 6 kev ua los ntawm nws cov tshuaj inhibitorslossis los ntawm depletion ntawm nws cov substrate-binding khub cyclin D, coj mus rau siab mTORC2. kev ua ub ua no kom pom cov tshuaj tiv thaiv kab mob (Daim duab 5).
Rb inhibit lub voj voog ntawm tes li cas?
Rb cov proteins tau xav tias yuav txwv tsis pub qhia E2F-tswj cov noob hauv ob txoj hauv kev (Dyson et al., 2002): los ntawm kev khi ncaj qha thiab thaiv qhov ua kom muaj zog ntawm E2F cov proteins los yog los ntawm kev tawm tsam los ntawm kev nrhiav neeg ua haujlwm ntawm HDAC, SWI / SNF yam, Polycomb pawg proteins (Dahiya li al., 2001) los yog methyltransferase (…
