Nature Search

Histamine receptors branch out

Stephen J. Hill
News & Views14 May 1987
Nature

Volume: 327, P: 104-105
Single cell transcriptomics and TCR reconstruction reveal CD4 T cell response to MHC-II-restricted APOB epitope in human cardiovascular disease

Atherosclerosis is accompanied by an autoimmune response that includes CD4 T cells recognizing epitopes in apolipoprotein B (APOB). Saigusa et al. analyzed the transcriptomes and T cell receptors of APOB-specific CD4 T cells by single-cell RNA sequencing using MHC-II tetramers in women with atherosclerosis, and showed that APOB-specific regulatory T cells switch to a more memory-like phenotype in atherosclerosis.

Ryosuke Saigusa
Payel Roy
Klaus Ley
Research12 May 2022
Nature Cardiovascular Research

Volume: 1, P: 462-475
H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Histone H2AX has a known role in DNA damage repair but interestingly, its loss is associated with resistance to poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-deficient tumours. Here, the authors identify a role of γH2AX in the degradation of replication forks and demonstrate that H2AX loss drives PARP inhibitor resistance via increased stressed fork stability in BRCA-deficient tumours.

Diego Dibitetto
Martin Liptay
Sven Rottenberg
ResearchOpen Access24 May 2024
Nature Communications

Volume: 15, P: 1-14
Cellularly active N-hydroxyurea FEN1 inhibitors block substrate entry to the active site

Structural, enzymatic and cellular target engagement studies reveal the mechanism of action by N-hydroxyurea small molecule inhibitors of the DNA repair enzyme, human flap endonuclease-1 (FEN1) that prevent cleavage of DNA flaps in cancer cells.

Jack C Exell
Mark J Thompson
Jane A Grasby
Research15 Aug 2016
Nature Chemical Biology

Volume: 12, P: 815-821
ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.

Gabriel Balmus
Domenic Pilger
Stephen P. Jackson
ResearchOpen Access08 Jan 2019
Nature Communications

Volume: 10, P: 1-18
The population requirement for cataract extraction: A cross-sectional study

Andrew Frost
Cherida Hopper
John Sparrow
Research01 Nov 2001
Eye

Volume: 15, P: 745-752
Arginine methylation regulates the p53 response

The tumour suppressor p53 is subject to complex regulation and arginine methylation is now shown to provide an additional level of control. The protein arginine methyltransferase (PRMT) 5 is recruited by Strap to methylate p53 in response to DNA damage, governing the p53 response.

Martin Jansson
Stephen T. Durant
Nicholas B. La Thangue
Research16 Nov 2008
Nature Cell Biology

Volume: 10, P: 1431-1439
International genome-wide meta-analysis identifies new primary biliary cirrhosis risk loci and targetable pathogenic pathways

Primary biliary cirrhosis is an autoimmune liver disease with poor therapeutic options. Here Cordell et al. a perform meta-analysis of European genome-wide association studies identifying six novel risk loci and a number of potential therapeutic pathways.

Heather J. Cordell
Younghun Han
Katherine A. Siminovitch
ResearchOpen Access22 Sept 2015
Nature Communications

Volume: 6, P: 1-11
Vision-related quality of life impairment in an elderly UK population: Associations with age, sex, social class and material deprivation

Andrew Frost
Jenny Eachus
Stephen Frankel
Research01 Nov 2001
Eye

Volume: 15, P: 739-744
Complete loss of ATM function augments replication catastrophe induced by ATR inhibition and gemcitabine in pancreatic cancer models

Charles R. Dunlop
Yann Wallez
Duncan I. Jodrell
ResearchOpen Access03 Aug 2020
British Journal of Cancer

Volume: 123, P: 1424-1436
Interactions of the DNA mismatch repair proteins MLH1 and MSH2 with c-MYC and MAX

Mary Mac Partlin
Elizabeth Homer
Robert Brown
Research13 Feb 2003
Oncogene

Volume: 22, P: 819-825

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