Vasquezbarlow3244

Proteins have evolved in specific 3D structures and play different functions in cells and determine various reactions and pathways. The newly synthesized amino acid chains once depart ribosome must crumple into three-dimensional structures so can be biologically active. This process of protein that makes a functional molecule is called protein folding. The protein folding is both a biological and a physicochemical process that depends on the sequence of it. In fact, this process occurs more complicated and in some cases and in exposure to some molecules like glucose (glycation), mistaken folding leads to amyloid structures and fatal disorders called conformational diseases. Such conditions are detected by the quality control system of the cell and these abnormal proteins undergo renovation or degradation. This scenario takes place by the chaperones, chaperonins, and Ubiquitin-proteasome complex. Understanding of protein folding mechanisms from different views including experimental and computational approaches has revealed some intermediate ensembles such as molten globule and has been subjected to biophysical and molecular biology attempts to know more about prevalent conformational diseases.Autophagy and apoptosis are catabolic pathways essential for homeostasis. They play a crucial role for normal placental and fetal development. These cell death mechanisms are exaggerated in placental disorders such as preeclampsia, intrauterine growth restriction (IUGR) and gestational diabetes mellitus (GDM). Apoptosis is widely studied, highly controlled and regulated whereas; autophagy is an orderly degradation and recycling of the cellular components. Cellular senescence may be initiated by a variety of stimuli, including hypoxia, oxidative stress, reduction in survival signals and nutrition deprivation. Apoptosis is regulated by two types of pathways intrinsic and extrinsic. Extrinsic pathway is initiated by apoptosis inducing cells such as macrophages, natural killer cells whereas; intrinsic pathway is initiated in response to DNA damage, cell injury and lack of oxygen. In autophagy, the cell or organelles undergo lysosomal degradation. Placental apoptosis increases as the gestation progresses while autophagy plays a role in trophoblast differentiation and invasion. In pregnancy disorders like preeclampsia and IUGR, proapoptotic markers such as caspase 3, 8, BAX are higher and antiapoptotic markers like Bcl-2 are lower. In GDM, apoptotic markers are reduced resulting in increased placental mass and fetal macrosomia. Apoptosis in the pathological pregnancies is also influenced by the reduced levels of micronutrients and long chain polyunsaturated fatty acids resulting in disturbed placental biology. This chapter describes the role of various key molecular events involved in cellular senescence and the various factors influencing them. This will help identify future therapeutic strategies for better management of these processes.Membraneless organelles (bodies, granules, etc.) are spatially distinct sub-nuclear and cytoplasmic foci involved in all the processes in a living cell, such as development, cell death, carcinogenesis, proliferation, and differentiation. Today the list of the membraneless organelles includes a wide spectrum of intranuclear and cytoplasmic bodies. Proteins with intrinsically disordered regions are the key players in the membraneless body assembly. However, recent data assume an important role of RNA molecules in the process of the liquid-liquid phase separation. High-level expression of RNA above a critical concentration threshold is mandatory to nucleate interactions with specific proteins and for seeding membraneless organelles. RNA components are considered by many authors as the principal determinants of organelle identity. Tandemly repeated (TR) DNA of big satellites (a TR family that includes centromeric and pericentromeric DNA sequences) was believed to be transcriptionally silent for a long period. Now we know about the TR transcription upregulation during gameto- and embryogenesis, carcinogenesis, stress response. In the review, we summarize the recent data about the involvement of TR RNA in the formation of nuclear membraneless granules, bodies, etc., with different functions being in some cases an initiator of the structures assembly. These RNP structures sequestrate and inactivate different proteins and transcripts. The TR induced sequestration is one of the key principles of nuclear architecture and genome functioning. Studying the role of the TR-based membraneless organelles in stress and disease will bring some new ideas for translational medicine.Acquired immunodeficiency syndrome (AIDS) has affected millions of people worldwide. The human immunodeficiency virus (HIV) which infects T cells by using CD4 as its main receptor. Currently different treatments are available against HIV infection which can improve life expectancy of the patient but still it remains incurable. CCR5, which is also required as a co-receptor by majority of HIV strains for entry into the target cells, is now being targeted for gene therapy to develop HIV resistance in patients. In this review, we discuss different strategies that are being adapted for CCR5-gene disruption in CD4+ T cells and in hematopoietic stem cells (HSCs) to generate a HIV-resistant immune system in infected individuals. If CCR5 gene that can shape HIV-resistant T cells, it will aim in new approaches in clinical trials. But these techniques have certain weaknesses and disadvantages, and will need to be paired with other strategies to form a full HIV remedy. C188-9 cost There is also a need to establish methods to help deter HIV re-emergence following targeted CCR5 therapy. But ultimately, this brought us a better knowledge of the road to HIV treatment.Numbers of pathogenic bacteria can induce apoptosis in human host cells and modulate the cellular pathways responsible for inducing or inhibiting apoptosis. These pathogens are significantly recognized by host proteins and provoke the multitude of several signaling pathways and alter the cellular apoptotic stimuli. This process leads the bacterial entry into the mammalian cells and evokes a variety of responses like phagocytosis, release of mitochondrial cytochrome c, secretion of bacterial effectors, release of both apoptotic and inflammatory cytokines, and the triggering of apoptosis. Several mechanisms are involved in bacteria-induced apoptosis including, initiation of the endogenous death machinery, pore-forming proteins, and secretion of superantigens. Either small molecules or proteins may act as a binding partner responsible for forming the protein complexes and regulate enzymatic activity via protein-protein interactions. The bacteria induce apoptosis, attack the human cell and gain control over various types of cells and tissue.