Nature Search

H4K16ac activates the transcription of transposable elements and contributes to their cis-regulatory function

Here, the authors show that chromatin at certain transposable elements (TEs) is coated with acetylation at H4K16, which can lead to increased local chromatin accessibility and transcription activation. In turn, these acetylated TEs display enhancer-like capabilities to regulate gene expression in cis.

Debosree Pal
Manthan Patel
Madapura M. Pradeepa
ResearchOpen Access12 Jun 2023
Nature Structural & Molecular Biology

Volume: 30, P: 935-947
In vitro generation of human cells with cancer stem cell properties

Cancer stem cells (CSCs) have been linked to the maintenance and progression of several tumours, but the properties of human CSCs are not well known. Reprogramming of human somatic cells during neoplastic in vitro transformation is shown to confer the properties of stem cells to primary differentiated fibroblasts. The cells that give rise to tumours in this case express the SSEA-1 antigen.

Paola Scaffidi
Tom Misteli
Research21 Aug 2011
Nature Cell Biology

Volume: 13, P: 1051-1061
Erratum: Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

Paola Scaffidi
Tom Misteli
Marco E. Bianchi
Amendments and Corrections30 Sept 2010
Nature

Volume: 467, P: 622
Disruption of the MSL complex inhibits tumour maintenance by exacerbating chromosomal instability

Monserrat et al. report that MSL inactivation suppresses tumour maintenance via enhancing chromosomal instability (CIN). Mechanistically, H4K16ac loss upon MSL inactivation generates under-replicated DNA, leading to CIN.

Josep Monserrat
Cristina Morales Torres
Paola Scaffidi
Research09 Apr 2021
Nature Cell Biology

Volume: 23, P: 401-412
Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis

Targeting self-renewing cancer cells without deleterious side effects in normal tissues has proven challenging. Here, the authors show that the well-tolerated HDAC inhibitor Quisinostat safely inhibits tumor maintenance and disease relapse by restoring high levels of histone H1.0.

Cristina Morales Torres
Mary Y. Wu
Paola Scaffidi
ResearchOpen Access14 Apr 2020
Nature Communications

Volume: 11, P: 1-15
Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

Paola Scaffidi
Tom Misteli
Research06 Mar 2005
Nature Medicine

Volume: 11, P: 440-445
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

Paola Scaffidi
Tom Misteli
Marco E. Bianchi
Research11 Jul 2002
Nature

Volume: 418, P: 191-195
Patient-specific cancer genes contribute to recurrently perturbed pathways and establish therapeutic vulnerabilities in esophageal adenocarcinoma

Identifying driver genes in unstable, heterogenous tumour types can be challenging. Here, Mourikis, Benedetti, Foxall and colleagues present a machine learning algorithm to tackle this problem in esophageal adenocarcinoma.

Thanos P. Mourikis
Lorena Benedetti
Francesca D. Ciccarelli
ResearchOpen Access15 Jul 2019
Nature Communications

Volume: 10, P: 1-17
Genome instability in progeria: when repair gets old

Genome instability and DNA repair defects have been discovered in the premature aging disease Hutchinson-Gilford progeria syndrome. These findings provide the first hint of a molecular mechanism for a group of human conditions caused by defects in the nuclear structural protein lamin A (pages 780–785).

Tom Misteli
Paola Scaffidi
News & Views01 Jul 2005
Nature Medicine

Volume: 11, P: 718-719
Bid acts on the permeability transition pore complex to induce apoptosis

Naoufal Zamzami
Chahrazed El Hamel
Guido Kroemer
Research14 Dec 2000
Oncogene

Volume: 19, P: 6342-6350
Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing

Paola Scaffidi
Tom Misteli
Research02 Mar 2008
Nature Cell Biology

Volume: 10, P: 452-459
ARID2 deficiency promotes tumor progression and is associated with higher sensitivity to chemotherapy in lung cancer

Thaidy Moreno
Beatriz Monterde
Ignacio Varela
Research19 Mar 2021
Oncogene

Volume: 40, P: 2923-2935
Second cancer in Philadelphia negative myeloproliferative neoplasms (MPN-K). A nested case-control study

Tiziano Barbui
Arianna Ghirardi
Guido Finazzi
Research29 May 2019
Leukemia

Volume: 33, P: 1996-2005
Benefit-risk profile of cytoreductive drugs along with antiplatelet and antithrombotic therapy after transient ischemic attack or ischemic stroke in myeloproliferative neoplasms

Valerio De Stefano
Alessandra Carobbio
Tiziano Barbui
ResearchOpen Access28 Feb 2018
Blood Cancer Journal

Volume: 8, P: 1-12
Reply to: Second primary malignancies in myeloproliferative neoplasms and the role of aspirin

Tiziano Barbui
Arianna Ghirardi
Alessandro Rambaldi
Correspondence07 Nov 2019
Leukemia

Volume: 34, P: 1208-1209

Search

H4K16ac activates the transcription of transposable elements and contributes to their cis-regulatory function

In vitro generation of human cells with cancer stem cell properties

Erratum: Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

Disruption of the MSL complex inhibits tumour maintenance by exacerbating chromosomal instability

Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis

Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

Patient-specific cancer genes contribute to recurrently perturbed pathways and establish therapeutic vulnerabilities in esophageal adenocarcinoma

Genome instability in progeria: when repair gets old

Bid acts on the permeability transition pore complex to induce apoptosis

Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing

ARID2 deficiency promotes tumor progression and is associated with higher sensitivity to chemotherapy in lung cancer

Second cancer in Philadelphia negative myeloproliferative neoplasms (MPN-K). A nested case-control study

Benefit-risk profile of cytoreductive drugs along with antiplatelet and antithrombotic therapy after transient ischemic attack or ischemic stroke in myeloproliferative neoplasms

Reply to: Second primary malignancies in myeloproliferative neoplasms and the role of aspirin

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