Phosphatidylinositol 3-kinase inhibition restores Ca2+ release defects and prolongs survival in myotubularin-deficient mice
Candice Kutchukian, Mirella Lo Scrudato, Yves Tourneur, Karine Poulard, Alban Vignaud, Christine Berthier, Bruno Allard, Michael W. Lawlor, Ana Buj-Bello, and Vincent Jacquemond
Myotubular myopathy is a fatal disease resulting from deficiency in the phosphoinositide phosphatase MTM1. Kutchukian et al. (2016) have now identified critical pathophysiological alterations of Ca2+ signaling which are involved in the disease and have revealed the benefit of a pharmacological treatment.
The Flexible Ends of CENP-A Nucleosome Are Required for Mitotic Fidelity.
Roulland Y, Ouararhni K, Naidenov M, Ramos L, Shuaib M, Syed SH, Lone IN, Boopathi R, Fontaine E, Papai G, Tachiwana H, Gautier T, Skoufias D, Padmanabhan K, Bednar J, Kurumizaka H, Schultz P, *Angelov D, *Hamiche A, *Dimitrov S.
CENP-A nucleosomal ends are highly flexible in solution, which prevents recruitment of the linker histone H1 thus allowing assembly of active kinetochore complex. Open CENP-A nucleosomal structure is essential for its mitotic function.
Macrophage PPARgamma, a Lipid Activated Transcription Factor Controls the Growth Factor GDF3 and Skeletal Muscle Regeneration.
Tamas Varga, Rémi Mounier, Andreas Patsalos, Péter Gogolák, Matthew Peloquin, Attila Horvath, Attila Pap, Bence Daniel, Gergely Nagy, Eva Pintye, Szilárd Poliska, Sylvain Cuvellier, Sabrina Ben Larbi, Brian E. Sansbury, Matthew Spite, Chester W. Brown, Bénédicte Chazaud, Laszlo Nagy
PPARγ is a lipid activated transcription factor essential for fat cells and linked to lipid processing in macrophages. Varga et al. (2016) now show that PPARγ is transcriptionally active and regulates the growth factor Gdf3 in repair macrophages in regenerating skeletal muscle, forming a paracrine axis connecting macrophages to muscle progenitor fusion.