The Genetics Society of America (GSA), founded in 1931, is the professional membership organization for scientific researchers and educators in the field of genetics. Our members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level.. Online ISSN: 1943-2631. ...

InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.

InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.

Pathological angiogenesis is the hallmark of diseases such as cancer and retinopathies. Although tissue hypoxia and inflammation are recognized as central drivers of vessel growth, relatively little is known about the process that bridges the two. In a mouse model of ischemic retinopathy, we found that hypoxic regions of the retina showed only modest rates of apoptosis despite severely compromised metabolic supply. Using transcriptomic analysis and inducible loss-of-function genetics, we demonstrated that ischemic retinal cells instead engage the endoplasmic reticulum stress inositol-requiring enzyme 1α (IRE1α) pathway that, through its endoribonuclease activity, induces a state of senescence in which cells adopt a senescence-associated secretory phenotype (SASP). We also detected SASP-associated cytokines (plasminogen activator inhibitor 1, interleukin-6, interleukin-8, and vascular endothelial growth factor) in the vitreous humor of patients suffering from proliferative diabetic retinopathy. ...

Cellular senescence is a complex phenotype observed in diverse tissues at distinct developmental stages. In adults, senescence likely acts to irreversibly prevent proliferation of damaged cells. Senescent cells appear during chronological aging, aberrant oncogene expression, and exposure to DNA damaging agents. Expression of the tumor suppressor p16INK4a increases with age in numerous mouse and human tissues and, thus, considered a reliable marker. Exposure to ionizing radiation (IR) leads to delayed increase in p16INK4a expression in mice tissues and cancer-treated patients Senescent cells accumulate in tissues and secrete a range of cytokines, chemokines, and proteases known as the senescence-associated secretory phenotype (SASP). Why senescent cells accumulate in vivo remains unclear. One theory suggests senescence accumulates with a decline in immune functions with age. While senescent cells support wound healing, accumulation of senescent cells also appears to contribute to tumor growth and ...

Communication between cells is quintessential for biological function and cellular homeostasis. Membrane-bound extracellular vesicles known as exosomes play pivotal roles in mediating intercellular communication in tumor microenvironments. These vesicles and exosomes carry and transfer biomolecules such as proteins, lipids and nucleic acids. Here we focus on exosomes secreted from senescent cells. Cellular senescence can alter the microenvironment and influence neighbouring cells via the senescence-associated secretory phenotype (SASP), which consists of factors such as cytokines, chemokines, matrix proteases and growth factors. This review focuses on exosomes as emerging SASP components that can confer pro-tumorigenic effects in pre-malignant recipient cells. This is in addition to their role in carrying SASP factors. Transfer of such exosomal components may potentially lead to cell proliferation, inflammation and chromosomal instability, and consequently cancer initiation. Senescent cells are ...

PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.

A Comparative Study of Associative Classifiers in Mesenchymal Stem Cell Differentiation Analysis: 10.4018/978-1-60960-067-9.ch011: Discovering how Mesenchymal Stem Cells (MSCs) can be differentiated is an important topic in stem cell therapy and tissue engineering. In a general context

Advancement of Sustainable Medical Innovations. There is declining productivity in biomedical research and development in terms of new product approvals, in part due to an inherently risk averse regulatory pathway for novel healthcare innovations. This is despite major achievements and opportunities in novel technological platforms. The portfolio of risk:benefit methodologies have been applied inconsistently and often conflated with cost-effective analysis. This yields results that do not effectively inform clinical practice or strategies for biomedical innovation. This investigation aims to assess risk:benefit appraisal methodologies in the analysis of published randomized controlled trials for pre-licensure biomedical.. Targeting the Senescence-Associated Secretory Phenotype, Buck Institute for Research on Aging. Senescent cells also develop resistance to signals for apoptosis (cellular suicide) and secrete inflammatory signaling molecules and protein-degrading enzymes into their local ...

Complete information for AXIN2 gene (Protein Coding), Axin 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

Although the induction of senescence in cancer cells is a potent mechanism of tumor suppression, senescent cells remain metabolically active and may secrete a broad spectrum of factors that promote tumorigenicity in neighboring malignant cells. Here we show that androgen deprivation therapy (ADT), a widely used treatment for advanced prostate cancer, induces a senescence-associated secretory phenotype in prostate cancer epithelial cells, indicated by increases in senescence-associated beta-galactosidase activity, heterochromatin protein 1 beta foci, and expression of cathepsin B and insulin-like growth factor binding protein 3. Interestingly, ADT also induced high levels of vimentin expression in prostate cancer cell lines in vitro and in human prostate tumors in vivo. The induction of the senescence-associated secretory phenotype by androgen depletion was mediated, at least in part, by down-regulation of S-phase kinase-associated protein 2, whereas the neuroendocrine differentiation of prostate ...

mesenchymal stem cell differentiation involved in metanephric nephron morphogenesis - Ontology Report - Chinchilla Research Resource Database

Loss of functionality during aging of cells and organisms is caused and accompanied by altered cell-to-cell communication and signalling. One factor thereby is the chronic accumulation of senescent cells and the concomitant senescence-associated secretory phenotype (SASP) that contributes to microenvironment remodelling and a pro-inflammatory status. While protein based SASP factors have been well characterized, little is known about small extracellular vesicles (sEVs) and their miRNA cargo. Therefore, we analysed secretion of sEVs from senescent human dermal fibroblasts and catalogued the therein contained miRNAs. We observed a four-fold increase of sEVs, with a concomitant increase of >80% of all cargo miRNAs. The most abundantly secreted miRNAs were predicted to collectively target mRNAs of pro-apoptotic proteins, and indeed, senescent cell derived sEVs exerted anti-apoptotic activity. In addition, we identified senescence-specific differences in miRNA composition of sEVs, with an increase of miR

Micromotion affects the tissue outcome at the peri-implant site. Interstitial fluid flow, induced by micromotion, may play a curtail part in the mesenchymal stem cell differentiation pathway necessary for bone regeneration. The aim of this project is to model the fluid flow at the peri-implant site composed of a soft tissue, for a glenoid implant for different gap sizes at physiological loading. Robberecht, Evert

Cellular senescence (deterioration) is a critical factor of biological aging that occurs in almost all peripheral tissues but little is known about its role in age-related neurodegenerative disorders, such as Parkinsons disease (PD). Senescence occurs in dividing cell types and halts cell proliferation (growth) in an irreversible manner. This process is caused by stress and puts cells at risk for tumor formation. Once established, these cells express a senescence-associated secretory phenotype (SASP), the pro-inflammatory secretion of cytokines and other factors that contribute to the age-related loss of peripheral tissue function. We aim to interrogate induction of senescence and SASP in response to alpha-synuclein (protein clumps) within the most prevalent dividing cell type in the brain, the astrocyte (cells that provide support and clean waste in the brain), and how this in turn affects dopaminergic cell health in relation to PD.. Hypothesis ...

TY - JOUR. T1 - Oxidative stress-induced senescence markedly increases disc cell bioenergetics. AU - Patil, Prashanti. AU - Falabella, Micol. AU - Saeed, Amal. AU - Lee, Dayeong. AU - Kaufman, Brett. AU - Shiva, Sruti. AU - Croix, Claudette St. AU - Van Houten, Ben. AU - Niedernhofer, Laura J.. AU - Robbins, Paul D.. AU - Lee, Joon. AU - Gwendolyn, Sowa. AU - Vo, Nam V.. PY - 2019/6. Y1 - 2019/6. N2 - Cellular senescence is a phenotype characterized by irreversible growth arrest, chronic elevated secretion of proinflammatory cytokines and matrix proteases, a phenomenon known as senescence-associated secretory phenotype (SASP). Biomarkers of cellular senescence have been shown to increase with age and degeneration of human disc tissue. Senescent disc cells in culture recapitulate features associated with age-related disc degeneration, including increased secretion of proinflammatory cytokines, matrix proteases, and fragmentation of matrix proteins. However, little is known of the metabolic ...

HMGB2 expression during chondrogenesis of human MSC. Immunohistochemistry shows that HMGB2 is expressed at days 1 and 3, but that expression is reduced at days 7, 14 upon induction of chondrogenesis. SO: safranin O staining. ...

Acts as a ventralizing factor during embryogenesis. Inhibits axin-mediated JNK activation by binding axin and disrupting axin homodimerization. This in turn antagonizes a Wnt/beta-catenin-independent dorsalization pathway activated by AXIN/JNK-signaling (By similarity ...

1. Bastonini E, Kovacs D, Picardo M. Skin pigmentation and pigmentary disorders: Focus on epidermal/dermal cross-talk. Ann Dermatol. 2016;28:279-89 2. Kim M, Han JH, Kim JH, Park TJ, Kang HY. Secreted frizzled-related protein 2 (sFRP2) functions as a melanogenic stimulator; The role of sFRP2 in UV-induced hyperpigmentary disorders. J Invest Dermatol. 2016;136:236-44 3. Coppé JP, Desprez PY, Krtolica A, Campisi J. The senescence-associated secretory phenotype: The dark side of tumor suppression. Annu Rev Pathol. 2010;5:99-118 4. Tchkonia T, Zhu Y, van Deursen J, Campisi J, Kirkland JL. Cellular senescence and the senescent secretory phenotype: Therapeutic opportunities. J Clin Invest. 2013;123:966-72 5. Kim YH, Choi YW, Lee JH, Soh EY, Kim JH, Park TJ. Senescent tumor cells lead the collective invasion in thyroid cancer. Nat Commun. 2017;8:15208 6. Mine S, Fortunel NO, Pageon H, Asselineau D. Aging alters functionally human dermal papillary fibroblasts but not reticular fibroblasts: A new view ...

Chronic obstructive pulmonary disease (COPD) is a highly prevalent and devastating condition for which no curative treatment is available. Exaggerated lung cell senescence may be a major pathogenic factor. Here, we investigated the potential role for mTOR signaling in lung cell senescence and alterations in COPD using lung tissue and derived cultured cells from patients with COPD and from age- and sex-matched control smokers. Cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype. To explore whether mTOR activation was a causal pathogenic factor, we developed transgenic mice exhibiting mTOR overactivity in lung vascular cells or alveolar epithelial cells. In this model, mTOR activation was sufficient to induce lung cell senescence and to mimic COPD lung alterations, with the rapid development of lung emphysema, pulmonary hypertension, and inflammation. ...

Component of the beta-catenin destruction complex required for regulating CTNNB1 levels through phosphorylation and ubiquitination, and modulating Wnt-signaling (By similarity). Controls dorsoventral patterning via two opposing effects; down-regulates CTNNB1 to inhibit the Wnt signaling pathway and ventralize embryos, but also dorsalizes embryos by activating a Wnt-independent JNK signaling pathway. In Wnt signaling, probably facilitates the phosphorylation of CTNNB1 and APC by GSK3B. Likely to function as a tumor suppressor. Facilitates the phosphorylation of TP53 by HIPK2 upon ultraviolet irradiation. Enhances TGF-beta signaling by recruiting the RNF111 E3 ubiquitin ligase and promoting the degradation of inhibitory SMAD7 (By similarity). Also component of the AXIN1-HIPK2-TP53 complex which controls cell growth, apoptosis and development.

Negative regulator of the canonical Wnt signaling pathway involved in neuroectodermal patterning. Acts by specifically binding phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), translocating to the cell membrane and interacting with key regulators of the canonical Wnt signaling pathway, such as components of the beta-catenin destruction complex ...

Human AXIN2 partial ORF ( NP_004646, 611 a.a. - 710 a.a.) recombinant protein with GST-tag at N-terminal. (H00008313-Q02) - Products - Abnova

Background: The role of mesenchymal stem cell in cellular therapy is the subject of interest for many researchers. The differentiation potential of MSCs and abilities in modulations of the recipients immune system makes them important cells in tissue regenerative studies. MSCs by releasing the proinflammatory cytokines play important role in immunomodulatory systems; however the signaling pathways for releasing of these mediators are not well understood. Glutathione has been shown to play a role in modulation of cytokines in hepatogenic differentiation. Objective: In the current study we aimed to investigate the effects of buthionine sulfoximine (BSO, inhibitor for glutathione synthesis) and N-acetylecystin (NAC, an inhibitor for ROS generation) on proinflammatory cytokines production in a hepatogenic differentiation model. Results: BSO and NAC significantly decreased IL-6 and TNF-α levels at 14 days of differentiation, whereas, NAC decreased the levels of IL-8 at days 2 and 14 of differentiation.

BMP-2 plays an essential role not only in embryonic stem cell differentiation, but also in mesenchymal stem cell differentiation and bone formation.

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To determine whether 1,25-dihydroxyvitamin D (1,25(OH)2 D) can exert an anti-osteoporosis role through anti-aging mechanisms, we analyzed the bone phenotype of mice with 1,25(OH)2 D deficiency due to deletion of the enzyme, 25-hydroxyvitamin D 1α-hydroxylase, while on a rescue diet. 1,25(OH)2 D deficiency accelerated age-related bone loss by activating the p16/p19 senescence signaling pathway, inhibiting osteoblastic bone formation, and stimulating osteoclastic bone resorption, osteocyte senescence, and senescence-associated secretory phenotype (SASP). Supplementation of exogenous 1,25(OH)2 D3 corrected the osteoporotic phenotype caused by 1,25(OH)2 D deficiency or natural aging by inhibiting the p16/p19 pathway. The proliferation, osteogenic differentiation, and ectopic bone formation of bone marrow mesenchymal stem cells derived from mice with genetically induced deficiency of the vitamin D receptor (VDR) were significantly reduced by mechanisms including increased oxidative stress, DNA ...

Mesenchymal stem cells (hMSC) represent a small population of cells located in bone marrow and most of the connective tissue. hMSC are multipotent and their ability to differentiate into osteoblast makes them suitable for application in regenerative orthopedics. In this research, I investigated the level of osteogenic differentiation of hMSC after the treatmant with osteoinductive molecules under the standard protocol. In vitro differentiation was evaluated by the analysis of bone markers - alkaline phosphatase and bonesialoprotein and by analysis of markers of stemness. Oct4, Sox2 i Nanog are pluripotency markers of embryonic stem cells but their expression was also confirmed in some types of adult stem cells. The aim of this research was to investigate if they were expressed in hMSC and if their expression decreases during differentiation. Results of RT qPCR showed that Oct4, Sox2 i Nanog are expressed in undifferentiated hMSC and that their expression decreases paralel with the apperance and ...

Looking for online definition of Beta catenin in the Medical Dictionary? Beta catenin explanation free. What is Beta catenin? Meaning of Beta catenin medical term. What does Beta catenin mean?

There are two genes that encode apc in Drosophila, apc 1 and 2. They are largely redundant, and only double mutants lead to strong pathway activation in embryos (Ahmed et al. 2002; McCartney et al. 2006). In apc1 apc2 double mutants, I assayed the ability of membrane-tethered apc2 to block signaling activation. As shown in Figure 1H, there was no real effect on the patterning of the cuticle. In contrast, expression of untethered apc2 rescued to a wild-type cuticle pattern (Figure 1G). I further used the apc1 apc2 double mutants to test the activity of both membrane-tethered and -untethered axin. Interestingly, expression of axin abolished signaling brought about by loss of both apc genes leading to a completely denticle-covered cuticle (Figure 1E). The tethered axin, however, was unable to overcome the loss of apc and signaling was not blocked (naked phenotype, Figure 1F).. To further assay the activity of the membrane-tethered and -untethered apc2 and axin, I expressed all four in a triple ...

Aqeilan, R. I., et al. (2005). WW domain-containing proteins, WWOX and YAP, compete for interaction with ErbB-4 and modulate its transcriptional function. Cancer Res. 65(15): 6764-72. 16061658 Alarcon, C., et al.. (2009). Nuclear CDKs drive Smad transcriptional activation and turnover in BMP and TGF-beta pathways. Cell 139(4): 757-69. PubMed Citation: 19914168 Aragón, E., et al. (2011). A Smad action turnover switch operated by WW domain readers of a phosphoserine code. Genes Dev. 25(12): 1275-88. PubMed Citation: 21685363 Azzolin, L., Panciera, T., Soligo, S., Enzo, E., Bicciato, S., Dupont, S., Bresolin, S., Frasson, C., Basso, G., Guzzardo, V., Fassina, A., Cordenonsi, M. and Piccolo, S. (2014). YAP/TAZ incorporation in the beta-Catenin destruction complex orchestrates the Wnt response. Cell 158: 157-170. PubMed ID: 24976009 Badouel, C., et al. (2009). The FERM-domain protein Expanded regulates Hippo pathway activity via direct interactions with the transcriptional activator Yorkie. Dev. ...

View Notes - 2011_Questions_Week_14_Answers from BIO 349 at University of Texas. 1. What happens when you deplete beta catenin in planarians? -The organism is no longer able to form a posterior side

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