Nat Commun: Short H2A histoprotein mutants express and manifest cancer protein properties in cancer

Nucleosomes are the basic sub-base of chromatin and consist of histone octomers (H2A, H2B, H3, and H4).
found single allegase mutations in histones, also known as "cancer proteins," in many different malignant tumors.
the proportion of cancer proteins in the total histogeneous library is very small, rarely through their own cause of cancer.
, it can work in synergy with other cancer genes to promote the development of tumor chromosome landscape.
recent large-scale cancer genome analysis identified relapsed mutations in the highly conservative histogeneic folding domain (HFD) in many common cancers.
these HFD mutations, including the well-characterized H2B-E76K mutation, reduce the stability of the nucleosome and interfere with chromatin.
SH2A (short histoprotein H2A mutant) is a group of histoprotein mutants expressed during sperm production in mammals.
is not yet clear about its expression regulation in normal testicles.
study, the researchers found that sH2A was associated with the regulation of unstable and alternating clipping mechanisms in nuclear small bodies.
H2A. B In a variety of cancers, the expression researchers by the species of short H2A sequence and wild H2A cancer protein-related mutations comparative analysis, the researchers found that sH2A protein has similar to the nuclear small body instability associated with the recurrence of cancer gene mutations, that is, with inherent cancer protein characteristics, the most typical sH2A mutation protein is H2A.B.
analysis of several existing cancer genomics data sets, the researchers found abnormal increases in sH2A in a variety of cancers.
further studies have shown that this expression is associated with the unique associated shear characteristics of the imbalance in the stability of the nucleosomes in these cancers.
analysis of shears in active cancers with H2A.B showed that the short H2A protein was a class of "off-the-shelf" cancer proteins whose abnormal expression can lead to chromatin dysfunction in cancer.