Soil salinization is one of the most important factors impacting plant productivity. About 3.6 billion of the world's 5.2 billion ha of agricultural dry land, have already suffered erosion, degradation, and salinization. Halophytes are typically considered as plants able to complete their life cycle in environments where the salt concentration is above 200 mM NaCl. Salinity adjustment is a complex phenomenon but essential mechanism to overcome salt stress, with both biophysical and biochemical implications. At this level, halophytes evolved in several directions, adopting different strategies. Otherwise, the lack of adaptation to a salt environment would negatively affect their electron transduction pathways and the entire energetic metabolism, the foundation of every plant photosynthesis and biomass production. The maintenance of ionic homeostasis is in the basis of all cellular counteractive measures, in particular in terms of redox potential and energy transduction. In the present work the biophysical mechanisms underlying energy capture and transduction in halophytes are discussed alongside with their relation with biochemical counteractive mechanisms, integrating data from photosynthetic light harvesting complexes, electron transport chains to the quinone pools, carbon fixation, and energy dissipation metabolism.
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http://dx.doi.org/10.3389/fpls.2014.00746 | DOI Listing |
Int J Surg
January 2025
Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
The immune response is modulated by a diverse array of signals within the tissue microenvironment, encompassing biochemical factors, mechanical forces, and pressures from adjacent tissues. Furthermore, the extracellular matrix and its constituents significantly influence the function of immune cells. In the case of carcinogenesis, changes in the biophysical properties of tissues can impact the mechanical signals received by immune cells, and these signals can be translated into biochemical signals through mechano-transduction pathways.
View Article and Find Full Text PDFMitochondria maintain a biochemical environment that cooperates with BH3-only proteins (e.g., BIM) to potentiate BAX activation, the key event to initiate physiological and pharmacological forms of apoptosis.
View Article and Find Full Text PDFUnlabelled: β-arrestins (βarrs) are key regulators of G protein-coupled receptors (GPCRs), essential for modulating signaling pathways and physiological processes. While current pharmacological strategies target GPCR orthosteric and allosteric sites, as well as G protein transducers, comparable tools for studying βarrs are lacking. Here, we present the discovery and characterization of novel small-molecule allosteric inhibitors of βarrs through comprehensive biophysical, biochemical, pharmacological, and structural analyses.
View Article and Find Full Text PDFNat Chem
January 2025
Department of Chemical and Biomolecular Engineering, University of California, Los Angeles, Los Angeles, CA, USA.
Understanding the emergence of complex biochemical systems, such as protein translation, is a great challenge. Although synthetic approaches can provide insight into the potential early stages of life, they do not address the equally important question of why the complex systems of life would have evolved. In particular, the intricacies of the mechanisms governing the transfer of information from nucleic acid sequences to proteins make it difficult to imagine how coded protein synthesis could have emerged from a prebiotic soup.
View Article and Find Full Text PDFProgrammed cell death (apoptosis) is essential part of the process of tissue regeneration that also plays role in the mechanism of pathology. The phenomenon of fast and transient permeability of mitochondrial membranes by various triggers, known as permeability transition pore (mPTP) leads to the release of proapoptotic proteins and acts as an initial step in initiation of apoptosis. However, a role for mPTP was also suggested for physiology and it is unclear if there is a threshold in number of mitochondria with mPTP which induces cell death and how this mechanism is regulated in different tissues.
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