ARC unleashes elastase

2021 ◽  
Vol 14 (677) ◽  
pp. eabi8030
Author(s):  
Annalisa M. VanHook

An antiapoptotic cytoplasmic protein becomes a proapoptotic nuclear protein in diabetes.

1990 ◽  
Vol 68 (2) ◽  
pp. 420-427 ◽  
Author(s):  
Arlette Nougarède ◽  
Pierre Rondet ◽  
Pierre Landré ◽  
Robert Saint-Côme

Following ablation of the main stem (decapitation), the mean nuclear protein content of the Pisum cotyledonary bud apical cells increased 35% as early as the 6th hour, just when a massive entry into the S phase was registered, and reached a maximum, with a 157% increase, at the 39th hour, when the mitotic activity was also at its highest. The ratio nuclear protein/nuclear DNA content was then multiplied by 1.8 in comparison with the ratio observed in the G0–1 noncycling nuclei of the inhibited cotyledonary bud. In the bud treated with cycloheximide, the mean nuclear protein content slowly increased following decapitation, but remained greatly inferior to that of the controls. A slight entry into the S phase was noticed at the 24th hour and the mean nuclear protein content, then maximal, increased 32% in comparison with the inhibited buds. In the control buds, the mean protoplasmic proteins content increased 116% at the 39th hour (maximal value), whereas it increased only 25% in the treated buds. Following treatment with cycloheximide, the entry into the S phase was postponed and of low amplitude. However, the recycling nuclei were able to divide. An increase in the mean nuclear and cytoplasmic protein content was a prerequisite if the entry into the S phase of G0–1, nuclei was not to be postponed.


2019 ◽  
Vol 20 (14) ◽  
pp. 1474-1485 ◽  
Author(s):  
Eyaldeva C. Vijayakumar ◽  
Lokesh Kumar Bhatt ◽  
Kedar S. Prabhavalkar

High mobility group box-1 (HMGB1) mainly belongs to the non-histone DNA-binding protein. It has been studied as a nuclear protein that is present in eukaryotic cells. From the HMG family, HMGB1 protein has been focused particularly for its pivotal role in several pathologies. HMGB-1 is considered as an essential facilitator in diseases such as sepsis, collagen disease, atherosclerosis, cancers, arthritis, acute lung injury, epilepsy, myocardial infarction, and local and systemic inflammation. Modulation of HMGB1 levels in the human body provides a way in the management of these diseases. Various strategies, such as HMGB1-receptor antagonists, inhibitors of its signalling pathway, antibodies, RNA inhibitors, vagus nerve stimulation etc. have been used to inhibit expression, release or activity of HMGB1. This review encompasses the role of HMGB1 in various pathologies and discusses its therapeutic potential in these pathologies.


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