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Downstream Signaling 1
Published in James E. Ferrell, Systems Biology of Cell Signaling, 2021
A similar sort of competition can happen whenever a high-affinity stoichiometric inhibitor is present in a pathway with a limited supply of upstream activator molecules, and stoichiometric inhibitors are quite common in signaling both at the level of ligand–receptor interaction and in downstream signaling. For example, the high-affinity µ-opioid receptor antagonist naloxone can compete with opioid agonists such as heroin, and so a sufficient dose of naloxone can block or reverse heroin intoxication (Figure 4.6b). In Drosophila EGF receptor signaling, the Argos protein binds to and sequesters the EGF-like protein Spitz; thus the receptor and Argos are competing for binding to Spitz/EGF (Figure 4.6c). Likewise, in cell cycle regulation, the cyclin-dependent kinases are regulated by a variety of high-affinity stoichiometric inhibitors, including the tumor suppressors p21Cip1, p27Kip1, p16INK4a, and p19INK4a. These can be viewed as competing with substrates for access to the active cyclin–Cdk complex (Figure 4.6d).
Virus-Based Nanobiotechnology
Published in Yubing Xie, The Nanobiotechnology Handbook, 2012
Magnus Bergkvist, Brian A. Cohen
The red clover necrotic mosaic virus (RCNMV) is a T = 3 symmetry plant virus that is a member of the Tombusviridae family. These viruses are typically carried by a vector (fungus, insects, etc.) and are mainly transmitted through soil. They are not capable of endosomal entry, instead they infect hosts cells when their vector cause mechanical damage to the root system. However, other physical application such as rubbing virus onto leaves also cause infection. The RCNMV virion has 23% nucleic acid and 77% protein content and is ∼36 nm in diameter with an ∼17 nm interior cavity (Musil and Gallo 1982, Sherman et al. 2006). Its RNA genome consists of one 3.9 kb polycistronic RNA-1 and a 1.45 kb monocistronic RNA-2 (both are single stranded and positive sense), wrapped around the surface interior. RNA-1 codes for three proteins: the capsid protein, p27—a polymerase-related protein, and p88—an RNA-dependent RNA polymerase. The RNA-2 codes for the protein, required for cell-to-cell movement. Interestingly, there are two distinct populations of the virus that are morphologically similar; one population contains four copies of RNA-2 and the second, biologically active population, has one copy each of RNA-1 and RNA-2 (Basnayake et al. 2006).
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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
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
Activated p53 then binds to the p21 promoter, thereby inactivating cyclin-CDKs in the G1 and S phases of the cell cycle. p21 is a cyclin-dependent kinase inhibitor (CKI) that binds to and inhibits the activity of cyclin-CDK2, CDK1, and CDK4/6 complexes, and therefore plays a crucial role in regulation of cell cycle progression at the G1 and S phases (Abbas and Dutta 2009; Wade Harper et al. 1993). In addition, p27 is another CKI called cyclin-dependent kinase inhibitor p27 (also known as KIP1), which inhibits activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, thus controlling cell cycle progression at the G1 phase (Chiarle, Pagano, and Inghirami 2000). In the present study, the cyclin-dependent kinase inhibitor p27 (p27KIP1) was also increased in SH-SY5Y cells after RF-EMF exposure (Figure 5c). Therefore, elevated p21 and p27 modified cyclin-CDK complexes, which blocked cell cycle progression at the G1 phase in SH-SY5Y cells after RF-EMF exposure (Figure 2).
Effects of tobacco compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on the expression of epigenetically regulated genes in lung carcinogenesis
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Sun Woo Jin, Jong Seung Im, Jae Hyeon Park, Hyung Gyun Kim, Gi Ho Lee, Se Jong Kim, Seung Jun Kwack, Kyu-Bong Kim, Kyu Hyuck Chung, Byung Mu Lee, Sam Kacew, Hye Gwang Jeong, Hyung Sik Kim
Hsf4 is a member of the heat shock transcription factor family, which contains conserved DNA binding and trimerization domains (Nakai et al. 1997). A potential role for Hsf4 is the regulation of cellular proliferation and differentiation (Hu and Mivechi 2006). In addition, Hsf4 deletion stimulates cellular senescence, which is associated with rise in expression of CDKIs p21 and p27 (Jin et al. 2012). Similarly, tumor development was significantly delayed in p53 and Hsf4 double-knockout mice compared with p53-null mice, indicating that Hsf4 is involved in cancer cell proliferation (Puustinen and Sistonen 2020).
Evaluation of anti-tumor activity of metformin against Ehrlich ascites carcinoma in Swiss albino mice
Published in Egyptian Journal of Basic and Applied Sciences, 2019
Om-Ali Elkhawaga, Sara Gebril, Nivin Salah
p21 is a downstream target gene of the tumor suppressor p53 [23]. It promotes cellular quiescence by arresting G1 progression under serum stimulation [24]. Metformin increased p21 expression. This is in agreement with [25],who observed that p53, p27 and p21 upregulation esophageal squamous cells carcinoma treated with metformin. Similarly,a single dose cisplatin upregulated p21 expression, the matter that confirmed by previous publications [26].