Zindy nielsen biography of mahatma gandhi
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The role of the p90 ribosomal S6 kinase family in prostate cancer progression and therapy resistance
Background
Prostate Cancer (PCa) is a major health problem and it is a leading cause of cancer-related death in men. In 2020, ~1.4 million new cases of PCa were diagnosed globally and nearly 500 thousand men died from the disease [1]. Treatments for organ-confined PCa include surgery and brachytherapy, and on average 87% of patients survive for 5 years or longer [2]. Tumor growth is usually dependent upon androgen, the male sex hormone, and hence patients with disease that has spread from the prostate capsule, are often treated with antiandrogens or luteinizing hormone-releasing hormone (LHRH) agonists. These aim to target the androgen signaling pathway, by blocking the Androgen Receptor (AR) or inhibiting androgen synthesis respectively. Although initially successful in the majority of patients, these therapies invariably fail and the tumor progresses to the aggressive Castration-Resistant Prostate Cancer (CRPC) stage. Few treatment options exist for CRPC and hence there is a need to identify novel therapeutic targets for this stage of the disease. A deep understanding of the signaling mechanisms that take place throughout disease progression is of paramount importance for
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Impaired ribosome biogenesis: mechanisms and aptness to crab and harmful
The tool was endorsed by representation Grant Intercession of interpretation Czech Position (17‐14743S brook 17-25976S), representation Internal Bestow of Palacky University (IGA‐LF‐2019-026) and say publicly European Regional Development Stock - Responsibilities ENOCH (No. CZ.02.1.01/0.0/0.0/16_019/0000868
References
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- 6. Wang W, Fault S, Zhang X, Wang MH, Wang H, Dynasty J, Zhang R. Ribosomal proteins instruct
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Abstract
Aging has emerged at the forefront of scientific research due to the growing social and economic costs associated with the growing aging global population. The defining features of aging involve a variety of molecular processes and cellular systems, which are interconnected and collaboratively contribute to the aging process. Herein, we analyze how telomere dysfunction potentially amplifies or accelerates the molecular and biochemical mechanisms underpinning each feature of aging and contributes to the emergence of age-associated illnesses, including cancer and neurodegeneration, via the perspective of telomere biology. Furthermore, the recently identified novel mechanistic actions for telomere maintenance offer a fresh viewpoint and approach to the management of telomeres and associated disorders. Telomeres and the defining features of aging are intimately related, which has implications for therapeutic and preventive approaches to slow aging and reduce the prevalence of age-related disorders.
Keywords: telomere dysfunction, TBDs, maintenance mechanisms, age-related disorders, therapeutic, aging hallmarks
Telomeres are genetic elements found at the terminal positions of linear chromosomes. The TTAGGG repeats that make up telomeric DNA in vertebrates are bound b