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Carbon Nanotubes for Drug Delivery Applications
Published in Ann Rose Abraham, Soney C. George, A. K. Haghi, Carbon Nanotubes, 2023
Jahanvee Mitra, G. K. P. Srilekha, Nilesh Wagh, Jaya Lakkakula
Earlier, it was discovered that cyclin A2 is a protein responsible for DNA replication, transcription, and regulating the cell cycle. On suppressing cyclin A2 by delivering siRNA, the proliferation of cancer cells can be controlled and apoptosis can be induced. Wang et al. applied the same strategy in their experiment by using functionalized single-walled CNTs mixed with siRNA (f-SWCNTs–siRNA), made out of a complementary strand of that of cyclin A2 producing gene. F-SWCNTs–siRNA of length 50–300 nm were analyzed by FT-IR and XPS and deployed for the treatment of chronic myelogenous leukemia cells (K562). Wang et al. reported that siRNA delivered by f-SWCNT was successful in suppressing cyclin A2 producing genes and eventually breaking the cycle of cancer cell division. This was one of the new strategies brought up by researchers in order to treat leukemia which is predicted to be used extensively in the coming future.71
Relaxation Oscillators
Published in James E. Ferrell, Systems Biology of Cell Signaling, 2021
The current view of regulatory circuit that drives the cell cycle is shown schematically in Figure 15.4. Oscillations are now know to be driven by the synthesis of several related mitotic cyclin proteins (cyclins B1α, B1β, B2, B4, B5, and A1, here collectively referred to as cyclin B). The cyclin B binds with high affinity to Cdk1, which is present in modest excess, and when the cyclin B–Cdk1 complex is in the right phosphorylation state, it is active as a protein kinase, phosphorylating hundreds of substrate proteins at many hundreds of phosphorylation sites. The collective effect of these phosphorylations is the dramatic cellular changes of mitotic entry, including chromatin condensation, nuclear envelope breakdown, vesiculation of the golgi, endoplasmic reticulum, and mitochondria, and reorganization of the microtubules into a football-shaped spindle.
Treatment Options for Chemical Sensitivity
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Kamp et al.468 showed that progression through the cell cycle requires the joint influence of positive regulator subunits, cyclins, and CDKs. These subunits regulate by phosphorylation a number of key substrates which subsequently activate a transition from G1 to S, and G2 to M phases of the cell cycle. Phosphate groups are transferred from ATP to a special amino acid in the target protein by protein kinases, while phosphatases remove the phosphate groups from the target proteins. The addition and removal of phosphate groups significantly affect the biochemical behavior of the target proteins. Many protein kinases and phosphatases have a specific affinity for their target proteins, and act as determinants for controlling the activity(s) of their target proteins. Indeed, ALF may possess these protein kinases which, acting as molecular switches, regulate an irregular T lymphocyte cell cycle to that of an ordered and orderly progression. Thus, helping the hypersensitivity being dampened or being thwarted.
Therapeutic potential of a 2,2’-bipyridine-based vanadium(IV) complex on HepG2 cells: cytotoxic effects and molecular targeting
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Eman Salah El-Shafey, Eslam Samy Elsherbiny
In the same context, the unlimited propagation of HCC cells could also refer to the uncontrolled progression of cell cycle, which is the main hallmark for numerous tumor cells [16]. Many cell cycle regulators are involved in this process. Cyclin D1 is considered as a critical cell cycle controller that mediates the G1/S-phase transition through triggering cyclin-dependent kinases such as Cdk4 and Cdk6 [17]. Additionally, Cyclin D1 can inhibit cell migration by the maintenance of p27kip1 and suppression of Rho-associated protein kinases and myosin [18]. Furthermore, Cyclin D1 could mediate indirect cell migration through limiting transition of epithelial-mesenchymal (EMT) [19]. Overexpression of cyclin D1 in liver cancer cells permits cellular proliferation through cell cycle activation and thus promotes tumor cell propagation. Thus, suppression of cyclin D1 level could be a potential strategy that aimed to inhibit progression of cancer cells [20].
Exposure to long-term evolution radiofrequency electromagnetic fields decreases neuroblastoma cell proliferation via Akt/mTOR-mediated cellular senescence
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Ju Hwan Kim, Sangbong Jeon, Hyung-Do Choi, Jae-Hun Lee, Jun-Sang Bae, Nam Kim, Hyung-Gun Kim, Kyu-Bong Kim, Hak Rim Kim
The cyclins bind to CDKs and then form cyclin-CDK complexes that predominantly regulate cell cycle progression (Wade Harper et al. 1993). Abbas and Dutta (2009) reported that CDK4 mainly controls the G1 phase, and that CDK2 and CDK1 regulate the S and M phases, respectively. To examine whether the rise in cyclin-CDK inhibitors p21 and p27 might be associated with the delay in G0/G1 following RF-EMF exposure, the protein expression levels of CDK1, CDK2, CDK4, and cyclin D were determined in SH-SY5Y cells. The protein expression levels of CDK2, CDK4, and cyclin D were significantly decreased after RF-EMF exposure (Figure 6b–d), with no marked change in CDK1 protein expression (Figure 6a).
Tetrazolo[1,5-a]pyrimidine-based metal(II) complexes as therapeutic agents: DNA interaction, targeting topoisomerase I and cyclin-dependent kinase studies
Published in Inorganic and Nano-Metal Chemistry, 2018
Azees Khan Haleel, Dharmasivam Mahendiran, Ummer Muhammed Rafi, Vijaykumar Veena, Sugumar Shobana, Aziz Kalilur Rahiman
Cyclin-dependent kinase (CDKs) controls the cell cycle progression, coordinating the eukaryotic cell division cycle and serves to integrate diverse growth-regulatory signals, and also strongly inhibit the tumor cell growth.[44,45] Based on the above facts, we have been interested to study the interactions of cyclin-dependent kinase (CDKs) receptor with copper(II) complexes (4–6).