Jennifer Hadley - Profile and Journalist Details
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Jennifer Hadley
Verified
Host, A Course in Miracles - Archive
Beats
video conferencing, Entertainment, Content Creator, disability technology, Epilepsy, Human rights
I don't cover macroeconomic, health issues, and politics (related to party politics).
Content
By Xiaowen Xie, Olivia Zhang, Ceejay Lee, N. Connor Payne, Leena Paul, Yiran Li, Hui Si Kwok, Hanjie Jiang, Jennifer Hadley, Vincenzo D’Angiolella, Philip Cole, Ralph Mazitschek, Paul A. Northcott, Ning Zheng, Melissa Batts, Pallavi M. Gosavi| Nature Verified AbstractCancer mutations can create neomorphic protein–protein interactions to drive aberrant function1,2. As a substrate receptor of the CULLIN3-RING E3 ubiquitin ligase complex, KBTBD4 is recurrently mutated in medulloblastoma3, the most common embryonal brain tumour in children4. These mutations impart gain-of-function to KBTBD4 to induce aberrant degradation of the transcriptional corepressor CoREST5. However, their mechanism remains unresolved.
By Jennifer Hadley, Mirza Yawar Baig, Chris Brennan Verified, Joyce Meyer| player.fm@ <% _(superChannels).chain().sortBy(function(c) { return } ).each(function(superchan) { %> <% inclusion = superchan.findInclusion(subChannel.id) %> <% }); %>
By Xiaowen Xie, Olivia Zhang, Ceejay Lee, N. Connor Payne, Leena Paul, Yiran Li, Hui Si Kwok, Hanjie Jiang, Jennifer Hadley, Vincenzo D’Angiolella, Philip Cole, Ralph Mazitschek, Paul A. Northcott, Ning Zheng, Melissa Batts, Pallavi M. Gosavi| Nature Verified AbstractCancer mutations can create neomorphic protein–protein interactions to drive aberrant function1,2. As a substrate receptor of the CULLIN3-RING E3 ubiquitin ligase complex, KBTBD4 is recurrently mutated in medulloblastoma3, the most common embryonal brain tumour in children4. These mutations impart gain-of-function to KBTBD4 to induce aberrant degradation of the transcriptional corepressor CoREST5. However, their mechanism remains unresolved.
Company Info
A Course in Miracles - Archive