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Hematopoietic stem cell expansion and generation: the ways to make a breakthrough.

Hematopoietic stem cell transplantation (HSCT) is the first field where human stem cell therapy was successful. Flooding interest on human stem cell therapy to cure previously incurable diseases is largely indebted to HSCT success. Allogeneic HSCT has been an important modality to cure various diseases including hematologic malignancies, various non-malignant hematologic diseases, primary immunodeficiency diseases, and inborn errors of metabolism, while autologous HSCT is generally performed to rescue bone marrow aplasia following high-dose chemotherapy for solid tumors or multiple myeloma. Re

Демиелинция производит сдвиг в населении кортикальных нейронов, которые синапсируют с каллосальными олигодендроцитными клетками.

Клетки потомства олигодендроцитов (ОРК) получают синаптическое воздействие от различных нейронов в мозгу развивающихся и взрослых. Понимание того, меняются ли нейронные популяции, которые синапируют с OPC в здоровом мозге в результате обезвоживания и/или ремиэлирования, может способствовать совершенствованию стратегий нейрозащиты или миелинового ремонта, разрабатываемых для демиелинизирующих заболеваний, таких, как множественный склероз. Чтобы изучить эту возможность, мы использовали трансгенную технологию крелокса, чтобы облегчить инфекцию ОПС модифицированным вирусом бешенства, что позволяет

Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.

Upon the induction of DNA damage, the chromatin structure unwinds to allow access to enzymes to catalyse the repair. The regulation of the winding and unwinding of chromatin occurs via epigenetic modifications, which can alter gene expression without changing the DNA sequence. Epigenetic mechanisms such as histone acetylation and DNA methylation are known to be reversible and have been indicated to play different roles in the repair of DNA. More importantly, the inhibition of such mechanisms has been reported to play a role in the repair of double strand breaks, the most detrimental type of DN

Harnessing live vectors for cancer vaccines: Advancing therapeutic immunotherapy.

Cancer vaccines represent a promising approach within immunotherapies. These vaccines are tailored to target tumor-specific antigens, thereby offering a precision approach to cancer treatment. The key principles in developing therapeutic cancer vaccines include identifying appropriate vaccine targets and selecting effective vaccine delivery platforms. These delivery platforms are diverse and have evolved to enhance the immune response. This review explores live cancer vaccines and the biological entities involved. Live cancer vaccines leverage the use of various biological entities to stimulat

Activin Receptor-Ligand Trap for the Treatment of β-thalassemia: A Serendipitous Discovery.

β-thalassemia is a hereditary disorder caused by defective production of β-globin chains of hemoglobin (Hb) that leads to an increased α/β globins ratio with subsequent free α-globins. Alpha globin excess causes oxidative stress, red blood cells membrane damage, premature death of late-stage erythroid precursors, resulting in ineffective erythropoiesis. The transforming growth factor β (TGF-β) superfamily signaling acts on biological processes, such as cell quiescence, apoptosis, proliferation, differentiation, and migration, and plays an essential role in regulating the hematopoiesis. This pa

Application of the CRISPR/Cas9-based gene editing technique in basic research, diagnosis, and therapy of cancer.

The 2020 Nobel Prize in Chemistry was awarded to Emmanuelle Charpentier and Jennifer Doudna for the development of the Clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease9 (CRISPR/Cas9) gene editing technology that provided new tools for precise gene editing. It is possible to target any genomic locus virtually using only a complex nuclease protein with short RNA as a site-specific endonuclease. Since cancer is caused by genomic changes in tumor cells, CRISPR/Cas9 can be used in the field of cancer research to edit genomes for exploration of the mechanisms of t

Расположение RNA на основе RiboTag обнаруживает олигодендроглиевую воспаление в аутоиммунном энцефаломиелите: последствия для патогенеза.

Клетки олигодендроглиевой линии (ООК) необходимы для миелинирования, ремиелиции и нейронной метаболической поддержки, но недавние данные указывают на то, что они также играют активную роль в нейроинфламмации. Цель этого исследования состояла в том, чтобы выявить подстрекательский транслатом ОРЦ в начале экспериментального аутоиммунного энцефаломиэлита (EAE) - широко используемой модели множественного склероза (MS) с использованием последовательности РНК на основе RNA, основанной на RiboTag. Мы пересекли мышей Риботага Olig2-Cre Мыши для получения экспресс-выражения реберосомного белка HA-тагон

РНК-Сек, базирующаяся на RNA-Seq, обнаруживает воспаление олигодендроглиевой линии в аутоиммунном энцефаломиелите.

Клетки олигодендроглиевой линии (ООК) имеют решающее значение для нейронных функций поддержки, включая минелинирование и воспоминание. Появляющиеся данные свидетельствуют об их активной роли в нейроинфламмации, особенно в таких условиях, как Множественный склероз (MS). В рамках этого исследования изучается возбудительный транслатом ОРЦ в начале экспериментального аутоиммунного энцефаломиелита (EAE), который представляет собой установленную модель НР. Использование последовательности РНК на основе RiboTag в генетически модифицированных системах Olig2-Cre Мыши RiboTag, мы опознали 1,556 Регулиру

Protein breakdown in muscle wasting: role of autophagy-lysosome and ubiquitin-proteasome.

Skeletal muscle adapts its mass as consequence of physical activity, metabolism and hormones. Catabolic conditions or inactivity induce signaling pathways that regulate the process of muscle loss. Muscle atrophy in adult tissue occurs when protein degradation rates exceed protein synthesis. Two major protein degradation pathways, the ubiquitin-proteasome and the autophagy-lysosome systems, are activated during muscle atrophy and variably contribute to the loss of muscle mass. These degradation systems are controlled by a transcription dependent program that modulates the expression of rate-lim

Муриновая корреляция саркомы Эпштейна-Барра и саркомы Капози (MHV-68) представляет собой ценную модель для оценки чувствительности к антивирусным препаратам и взаимодействия в комбинаторных наркотиках.

Человеческие герпесвирусы представляют собой основные человеческие патогены. Особый интерес представляют члены подсемейства < < Герпесвирина > > , поскольку они вызывают хронические заболевания, такие, как рак, изменяя клеточные процессы и вводя клетки отдыха в непрерывно расширяющуюся фазу. Кроме того, в центре внимания постоянно находятся аутоиммунные заболевания, такие, как множественный склероз. Прототипический вирус человека - герпесвирус - вирус Эпштейна - Барра (ЭБВ) оказался трудно проанализировать в целях развития противовирусной терапии из-за проблем, связанных с распрост

Моноцитная система снижает эффективность центральной нервной системы ремиелиции.

Регенерация миелина в центральной нервной системе (СНС) восстанавливает нервное здоровье и функции, однако снижение ее эффективности в результате старения и развития нейродегенеративных заболеваний ведет к потере аксона и/или дегенерации. Несмотря на то, что миелиоидные клетки CNS были причастны к регулированию эффективности ремиелиции, не ясно, какой конкретный вклад вносят моноциты крови по сравнению с микроглией. Здесь мы обнаруживаем, что моноциты выполняют функции, не связанные с избытком, по сравнению с микроглией в регулировании ремиэлизации. Используя трансгенную мышь, в которой класси

Immune System and DNA Repair Defects in Ovarian Cancer: Implications for Locoregional Approaches.

In the last few years, substantial progress has been made in the treatment of ovarian cancer, with increased knowledge about the biology of the disease. Ovarian cancer is a neoplasm strongly linked to defects in DNA repair mechanisms, where deficiency in the homologous recombination (HR) system results in a better response of ovarian cancers to therapy, whether platinum-based chemotherapy, anthracyclines, or poly (ADP-ribose) polymerase (PARP) inhibitors. More recently, it has been demonstrated that different ovarian cancer histotypes may have different immunogenicity. Interestingly, defects i

Совпадение в полном тексте источника
… The main reactions in HR are catalyzed by the Rad51/RecA family DNA recombinases [ 37 ]. …

Mapping oncogenic protein interactions for precision medicine.

Normal protein-protein interactions (normPPIs) occur with high fidelity to regulate almost every physiological process. In cancer, this highly organised and precisely regulated network is disrupted, hijacked or reprogrammed resulting in oncogenic protein-protein interactions (oncoPPIs). OncoPPIs, which can result from genomic alterations, are a hallmark of many types of cancers. Recent technological advances in the field of mass spectrometry (MS)-based interactomics, structural biology and drug discovery have prompted scientists to identify and characterise oncoPPIs. Disruption of oncoPPI inte

Совпадение в полном тексте источника
… Small‐molecule inhibitors that target protein‐protein interactions in the RAD51 family of recombinases. ChemMedChem. 2015;10(2):296‐303. …

Circadian clock and cancer.

Circadian rhythms play a critical role in regulating physiological and behavioral processes, such as the sleep-wake cycle, hormone secretion, and metabolism. These rhythms are controlled by endogenous biological clocks, which are synchronized with environmental cues, primarily the light-dark cycle. Notably, disruption or reprogramming of circadian rhythms is closely associated with cancer initiation, progression, and treatment response. At the molecular level, the dysregulation of core clock genes can disturb normal cellular rhythms, leading to aberrant cell proliferation, impaired DNA repair,

The role of lncRNA NEAT1 in human cancer chemoresistance.

Chemotherapy is currently one of the most effective methods in clinical cancer treatment. However, chemotherapy resistance is an important reason for poor chemotherapy efficacy and prognosis, which has become an urgent problem to be solved in the field of cancer chemotherapy. Therefore, it is very important to deeply study and analyze the mechanism of cancer chemotherapy resistance and its regulatory factors. Long non-coding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) has been shown to be closely associated with chemotherapy resistance in cancer. NEAT1 induces cancer cell resi

Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory disease that leads to myelin loss and neurological dysfunction. Clinical studies show increased anti-Kir4.1 antibody levels in MS patients' serum, indicating its diagnostic potential. However, the specific mechanism has remained elusive. In a mouse model of experimental autoimmune encephalomyelitis (EAE), it is found that impaired Kir4.1 channels in oligodendrocyte precursor cells (OPCs) hindered myelin repair in the spinal cord. Using a thermal shift assay (TSA), the small molecule 2-D08 is identified, which effectively activated Kir4.1 channe

Collateral Victim or Rescue Worker?-The Role of Histone Methyltransferases in DNA Damage Repair and Their Targeting for Therapeutic Opportunities in Cancer.

Disrupted DNA damage signaling greatly threatens cell integrity and plays significant roles in cancer. With recent advances in understanding the human genome and gene regulation in the context of DNA damage, chromatin biology, specifically biology of histone post-translational modifications (PTMs), has emerged as a popular field of study with great promise for cancer therapeutics. Here, we discuss how key histone methylation pathways contribute to DNA damage repair and impact tumorigenesis within this context, as well as the potential for their targeting as part of therapeutic strategies in ca

Animal Models of Multiple Myeloma Bone Disease.

Multiple myeloma (MM) is a clonal B-cell disorder characterized by the proliferation of malignant plasma cells (PCs) in the bone marrow, the presence of monoclonal serum immunoglobulin, and osteolytic lesions. It is the second most common hematological malignancy and considered an incurable disease despite significant treatment improvements. MM bone disease (MMBD) is defined as the presence of one or more osteolytic bone lesions or diffused osteoporosis with compression fracture attributable to the underlying clonal PC disorder. MMBD causes severe morbidity and increases mortality. Cumulative

Advances in CRISPR-Cas technology and its applications: revolutionising precision medicine.

CRISPR-Cas (Clustered Regularly Interspaced Short Palindromic Repeats-CRISPR-associated proteins) has undergone marked advancements since its discovery as an adaptive immune system in bacteria and archaea, emerged as a potent gene-editing tool after the successful engineering of its synthetic guide RNA (sgRNA) toward the targeting of specific DNA sequences with high accuracy. Besides its DNA editing ability, further-developed Cas variants can also edit the epigenome, rendering the CRISPR-Cas system a versatile tool for genome and epigenome manipulation and a pioneering force in precision medic

Совпадение в полном тексте источника
… Recently, researchers fused Cas9 with recombinases, such as Rad51 or RAD52, which enhance homology-directed repair (HDR) by promoting alignment and integration of donor DNA templates at Cas9-induced DSBs ( Tran et al., 2019 ). …

Abstracts from 2020 national congress of the Italian Society of Hypertension (SIIA).

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