From 756e63652f11155c3638f8a42892cc7ce3138970 Mon Sep 17 00:00:00 2001 From: Charles Date: Wed, 23 Oct 2019 13:09:14 +0900 Subject: [PATCH] In PNAS today. --- biblio/31591214.mdwn | 10 ++++++++++ 1 file changed, 10 insertions(+) create mode 100644 biblio/31591214.mdwn diff --git a/biblio/31591214.mdwn b/biblio/31591214.mdwn new file mode 100644 index 00000000..d83566e2 --- /dev/null +++ b/biblio/31591214.mdwn @@ -0,0 +1,10 @@ +[[!meta title="Human papillomavirus 16 promotes microhomology-mediated end-joining."]] +[[!tag HPV not_read]] + +Proc Natl Acad Sci U S A. 2019 Oct 7. pii: 201906120. doi:10.1073/pnas.1906120116 + +Leeman JE, Li Y, Bell A, Hussain SS, Majumdar R, Rong-Mullins X, Blecua P, Damerla R, Narang H, Ravindran PT, Lee NY, Riaz N, Powell SN, Higginson DS. + +Human papillomavirus 16 promotes microhomology-mediated end-joining. + +[[!31591214 desc="“Compared to HPV-negative HNSCC genomes, HPV+ cases demonstrated a marked increase in the proportion of deletions with flanking microhomology, a signature associated with a backup, error-prone double-strand break repair pathway known as microhomology-mediated end-joining (MMEJ). Then, using 3 different methodologies to comprehensively profile double-strand break repair pathways in isogenic paired cell lines, we demonstrate that the HPV16 E7 oncoprotein suppresses canonical nonhomologous end-joining (NHEJ) and promotes error-prone MMEJ, providing a mechanistic rationale for the clinical radiosensitivity of these cancers.”"]] -- 2.47.3