Postepy biochemii (Postepy Biochem)

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Website Postepy Biochemii website
Other titles Postepy biochemii
ISSN 0032-5422
OCLC 301567728
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Huntington's disease is a progressive neurodegenerative disorder of genetic origin that still lacks an effective treatment. Recently, a number of new attempts have been undertaken to develop a successful molecular therapy for this incurable condition. The novel approaches employ, among others, some new methods to selectively silence the mutated gene or to neutralize its toxic protein product. This paper reviews all major strategies that are currently considered for molecular therapy of Huntington's disease while discussing their potential effectiveness regarding the treatment of both the Huntington's disease and a large group of related neurodegenerative disorders associated with abnormal protein aggregation.
    Postepy biochemii 08/2015; 61(1):18-24.
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    ABSTRACT: Within the last decade, several antimicrobial peptides (AMPs) have been discovered. Cathelicidins are one family of AMPs characterized by a conserved cathelin domain and a variable C-terminal cationic antimicrobial domain. These peptides are produced by different cells, including leukocytes, epithelial cells and keratinocytes. Besides their direct antimicrobial function, cathelicidins can also regulate the course of inflammation and influence the mechanisms of innate immunity. In this review we discuss the biology of animal cathelicidins, their structure, expression and function.
    Postepy biochemii 08/2015; 61(1):93-101.
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    ABSTRACT: Almost six decades of studies explained many aspects of cytokinin complex metabolism, such as, biogenesis, degradation, signal perception and interaction with other phytohormones (mainly with auxins). A dual character of cytokinins' action on the nuclear genes (activation and repression) has been explained by recognition of the two types on nuclear receptors, which ensure a precise mechanism of self-control. Cytokinins promote the process of photosynthesis at different levels of plant- and cellular organization (development of leaves and plastids, influence on the photosynthetic proteins, activation of photosynthetic genes, etc.). An anti-senescing action of these hormones has been recently attributed to the activation of intra-cellular invertase, which suppress floem loading and change the sink-source pattern of the leaf.
    Postepy biochemii 08/2015; 61(1):61-8.
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    ABSTRACT: Numerous studies have revealed that MDM2 oncoprotein is upregulated in different types of cancer. Additionally, it was demonstrated that in some cases, MDM2 may inhibit the neoplastic transformation process. In other words, MDM2 protein can be considered as an oncogene or as a tumor suppressor depending on the appropriate cellular context. MDM2 functions on different levels in the cell, which is a consequence of its complex structure, a plethora of interacting partners and regulation through numerous postranslational modifications. Thus, an alteration of the delicate balance in MDM2 activity can influence transformation and cancer development. Genomic instability is a hallmark of cancer, which inversely correlates to the activity of DNA damage response. In the case of not transformed cells MDM2 inhibits double strand brakes (DSBs) repair, hence stimulating carcinogenesis. In cancer cells MDM2 stimulates cytostatic-induced DSBs repair, thus leading to chemoresistance.
    Postepy biochemii 08/2015; 61(1):42-51.
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    ABSTRACT: Torsin 1A is a protein mutated in torsion dystonia type 1, a hereditary neurological disorder of early onset and variable clinical picture. The basic cellular function of torsin 1A, a polypeptide localized predominantly in the endoplasmic reticulum and nuclear envelope, remains unknown, although the protein is suspected of being involved in many different cellular processes, including regulating a proper structure and function of nuclear envelope, contributing to the synaptic vesicular trafficking, or assisting in proper folding of misfolded proteins. This review summarizes the current state of knowledge regarding the potential functions of torsin 1A in the context of hypothetical pathomechanisms responsible for torsion dystonia type 1.
    Postepy biochemii 08/2015; 61(1):35-41.
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    ABSTRACT: Arabidopsis thaliana since a few decades is used as a model for biological and plant genetic research. Natural variation of this species is related to its geographical range which covers different climate zones and habitats. The ability to occupy such a wide area by Arabidopsis is possible due to its stress tolerance and adaptability. Arabidopsis accessions exhibit phenotypic and genotypic variation, which is a result of adaptation to local environmental conditions. During development, plants are subjected to various stress factors. Plants show a spectrum of reactions, processes and phenomena that determine their survival in these adverse conditions. The response of plants to stress involves signal detection and transmission. These reactions are different and depend on the stressor, its intensity, plant species and life strategy. It is assumed that the populations of the same species from different geographical regions acclimated to the stress conditions develop a set of alleles, which allow them to grow and reproduce. Therefore, the study of natural variation in response to abiotic stress among Arabidopsis thaliana accessions allows to find key genes or alleles, and thus the mechanisms by which plants cope with adverse physical and chemical conditions. This paper presents an overview of recent findings, tools and research directions used in the study of natural variation in Arabidopsis thaliana accessions. Additionally, we explain why accessions can be used in the phylogenetic analyses and to study demography and migration of Arabidopsis thaliana.
    Postepy biochemii 08/2015; 61(1):102-13.
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    ABSTRACT: Recent studies reveal that estrogens act on cells and tissues, not only through two canonical estrogen receptors ERα and ERβ, but also through the receptor coupled with G proteins, named GPER, formerly GPR30, and member of seven transmembrane receptor superfamily. GPER was found to be implicated both in rapid non-genomic estrogen response and in transcriptional regulation. Effects of GPER include activation of MAPK and PI3K signaling pathways, stimulation of adenyl cyclase, and mobilization of calcium ions from intracellular stores, as well as upregulation of genes such as FOS and CTGF. Identification of agonists and antagonists of GPER allowed not only to shed light on the participation of estrogen signaling in the biology and pathobiology of hormone-dependent tissues, but also its importance in the estrogen and antiestrogen therapies. Antiestrogens tamoxifen, raloxifene, or fulvestrant proved,to be agonists of GPER, which undoubtedly is not without significance for the efficacy of the therapy.
    Postepy biochemii 08/2015; 61(1):52-60.

  • Postepy biochemii 03/2015; 60(4):418-23.
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    ABSTRACT: Ageing leads to irreversible alterations in the nervous system, which to various extent impair its functions such as capacity to learn and memory. In old neurons and brain, similarly to what may take place in other cells, there is increased oxidative stress, disturbed energetic homeostasis and metabolism, accumulation of damage in proteins and nucleic acids. Characteristic of old neurons are alterations in plasticity, synaptic transmission, sensitivity to neurotrophic factors and cytoskeletal changes. Some markers of senescence, whose one of them is SA-beta-galactosidase were used to show the process of neuronal ageing both in vitro, and in vivo. Some research suggest that, despite the fact that neurons are postmitotic cells, it is cell cycle proteins which play a certain role in their biology, e.g. differentiation. However, their role in neuronal ageing is not known or explained. Ageing is the serious factor of development of neurodegenerative diseases among others Alzheimer disease.
    Postepy biochemii 08/2014; 60(2):177-86.
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    ABSTRACT: Development of the civilization and medicine enables an even longer lifespan of people. To modulate the aging process it is necessary to discover its molecular mechanism and its causes. It has been known for almost 60 years that cells undergo senescence. A lot of markers of senescence have been described to distinguish senescent cells. Every year we can observe an increase in the number of data, supporting the thesis that the reason for aging of the whole organism is cellular senescence. We age because cells building tissues and organs undergo senescence. It is also believed that cellular senescence can increase the frequency of age-related diseases. The role of cellular senescence strictly depends on the age of the individual. In young ones it is essential for: protection against cancer and tissue regeneration. In old ones it causes tissues and organs dysfunctions and leads to age-related diseases. Slowing down aging could prevent age-related diseases and this seems to be more promising than curing them. To enrich our knowledge concerning aging it is important to understand signaling pathways leading to senescence. Recently a new role of cellular senescence has been discovered, namely during embryogenesis. This observation is very surprising and shows a new face of cellular senescence. It is possible that, similarly to the previously described role of apoptosis in embryogenesis, senescence is indispensable for proper organogenesis. Cellular senescence seems to be the universal and fundamental process, the role of which changes during the lifespan.
    Postepy biochemii 08/2014; 60(2):147-60.
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    ABSTRACT: Cellular senescence is the process that lead to terminal growth arrest induced by unrepairable double strand DNA damage (DSB). Moreover, activation of the oncogenes as well as inhibition of the tumor suppressor genes were shown to contribute to senescence induction and the senescent cells were identified in the premalignant lesions. Thus senescence is considered as an natural antitumor barrier that act at the early stages of cancerogenesis to stop the proliferation of transformed cells. Interestingly, the premalignant cells that escaped senescence and progress into full blown tumor cells still remain sensitive to induction of senescence, for example during chemio- or radiotherapy. Thus, induction of cancer cell senescence, similarly to apoptosis, is considered to restrain tumor growth and thus contribute to effectiveness of anticancer therapy. The senescent cells, although do not proliferate, remain viable and metabolically active. They secret a lot of cytokines, mitogens as well as enzymes degrading extracellular matrix. These factors can have opposing effect on neighboring cells, leading to senescence induction or stimulation of proliferation. Thus, senescence can act as an double edge sword that inhibit the propagation of potentially dangerous, transformed cells on one hand or induce cell division of the same cell on the other. Presently a lot of work is focused on finding new therapeutic strategies that would involve the tumor targeted senescence induction in both early late stages of cancer development. Nevertheless, the unwanted influence of the senescent cells on the microenvironment, requires careful monitoring the effects of pro-senescent therapies in each case.
    Postepy biochemii 08/2014; 60(2):194-206.