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Macromolecular Absorption From The Digestive Tract In Young Vertebrates
Published in Károly Baintner, Intestinal Absorption of Macromolecules and Immune Transmission from Mother to Young, 2019
In phase 2, a “triggering” mechanism functions. The major rise of sucrase is not affected by glucocorticoid treatment, adrenalectomy, or diet (weaning) if the rise has once begun. The rise or decrease of different glucocorticoid-sensitive enzymes occur simultaneously in coordination.553 The disappearance of vacuolation seems to be somewhat delayed as compared to the rise of sucrase and the suppression of IgG transmission, and the difference may be explained by the somewhat slower turn-over of the distal epithelium as compared to that of the proximal small intestine. Another possible explanation may be a proximodistal difference in the threshold hormone level. From about day 17 on (beginning of phase 2), sucrase activity does not respond to exogenous glucocorticoids or the elimination of the endogenous hormone. In other words, the reversible process becomes irreversible, and this condition is preserved until the end of the life. Maturation of gastric oxyntic cells1126 and closure of the distal gut301 follows a similar pattern.
General and Practical Aspects of Membrane Protein Crystallization
Published in Hartmut Michel, Crystallization of Membrane Proteins, 1991
The speed used to achieve supersaturation should also be varied. During crystallization attempts the membrane protein can undergo several competing reactions. These are indicated in Figure 5. It may be denatured, which is an irreversible process (i). It may form an amorphous precipitate without loss of activity and without apparent denaturation (ii). This is a reversible process. We hope that the membrane protein crystallizes (iii). This again is a reversible process. Long term experiments favor process (i), whereas fast experiments (rapid supersaturation) favor process (ii). Crystals are frequently obtained only on the intermediate time-scale.
Section IV
Published in Evan A. Evans, Richard Skalak, Mechanics and Thermodynamics of Biomembranes, 1980
A perfectly elastic material obeys Equation 4.2.3 at constant temperature. External forces, which deform an elastic material, do work on the material that depends only on the initial and final state of deformation. The heat exchange produced during the deformation is completely recovered when the external forces are removed and the material returns to its initial state. However, deformation of any real material will take place over a finite period of time, and internal heat dissipation will occur due to the frictional interaction of molecules. In an actual process, irrecoverable heat exchange may result. Therefore, Equations 4.2.5 can only be approached in the limit, where dissipation is negligible. Another essential requirement for a reversible process is that there be no irreversible material alterations (e.g., molecular rearrangements). Permanent structural changes will occur in proportion to the magnitude and duration of the external forces. Consequently, the forces must be applied and removed such that the structure does not have time to relax to a new material configuration. It may be impossible for a given process to satisfy both requirements simultaneously, i.e., a slow enough deformation of the material to have negligible dissipation and fast enough to avoid structural change.
Hepatic stellate cell reprogramming via exosome-mediated CRISPR/dCas9-VP64 delivery
Published in Drug Delivery, 2021
Nianan Luo, Jiangbin Li, Yafeng Chen, Yan Xu, Yu Wei, Jianguo Lu, Rui Dong
Liver fibrosis is the pathological reaction of various chronic pathogenic factors acting on the liver and causing tissue injury and repair, and it is the necessary stage of the development of many liver diseases to cirrhosis (Forbes & Newsome, 2016; Kyritsi et al., 2020). Studies have shown that hepatic fibrosis is a reversible process (Deng et al., 2018; Zhang et al., 2020). In recent years, with the development of molecular biology and the elucidated mechanism of liver fibrosis, gene therapy is expected to be an effective anti-liver fibrosis method. Gene therapy for hepatic fibrosis mainly plays a role in preventing the development of fibrosis, stimulating the division of liver cells and the reconstruction of liver tissue structure (Iredale, 2004; Greuter & Shah, 2019; Choi et al., 2020).
Role of co- and post-translational modifications of SFKs in their kinase activation
Published in Journal of Drug Targeting, 2020
Mei-Lian Cai, Meng-Yan Wang, Cong-Hui Zhang, Jun-Xia Wang, Hong Liu, Hong-Wei He, Wu-Li Zhao, Gui-Ming Xia, Rong-Guang Shao
During palmitoylation, a palmitoyl group (derived from palmitic acid) is post-translationally added to the cysteine, with less added to serine and threonine. This modification is a dynamic and reversible process. Acyltransferases (PATs) mediate the process. Although myristoylation is essential to membrane anchorage of SFKs [32], myristoylation alone is not sufficient for membrane anchorage, and membrane anchorage still requires other modifications such as palmitoylation (in most SFKs) or a polybasic cluster (in Src) to finish collaboratively [41,42], and the effect of palmitoylation as a second signal to membrane anchorage is stronger than the polybasic cluster [43]. Of note, myristoylation is a prerequisite for the palmitoylation of SFKs. With the exception of Src and Blk, all SFKs are palmitoylated at Cys3, Cys5 or Cys6 in the SH4 domain [32,44]. Lyn and Yes are mono-palmitoylated at Cys3, Fyn is dual-palmitoylated at Cys3 and Cys6, and Lck is dual-palmitoylated at Cys3 and Cys5. Palmitoylation at cysteine affects SFKs activity by regulating the trafficking, localisation and stability of SFKs [45,46].
The double-edged role of IL-22 in organ fibrosis
Published in Immunopharmacology and Immunotoxicology, 2020
Jia Chen, RathnaSilviya Lodi, Shiqing Zhang, Zhaoliang Su, Yan Wu, Lin Xia
Although fibrosis is associated with high mortality, it is also a reversible process and a repair mechanism. Fibrosis can form scars instead of damaged tissues in the initial stage, but in the middle and late stages, fibrosis can accelerate the development of diseases, leading to organs failures. Different microenvironments that are associated with inflammation may contribute to the double-edged roles of IL-22 and the cellular and molecular mechanisms underlying these events should be studied further. Besides, IL-22 together with its receptors, may be used to develop new therapeutic strategies for fibrotic diseases, which may make clinical treatment possible using IL-22 as a potential target.