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Добірка наукової літератури з теми "3101 Biochemistry and cell biology"

Автор: Grafiati

Опубліковано: 10 січня 2023

Оновлено: 28 січня 2023

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Статті в журналах з теми "3101 Biochemistry and cell biology"

Prabhala, Rao H., Paola Neri, Jooeun E. Bae, Pierfrancesco Tassone, Masood A. Shammas, Charles K. Allam, John F. Daley, et al. "Dysfunctional T regulatory cells in multiple myeloma." Blood 107, no. 1 (January 1, 2006): 301–4. http://dx.doi.org/10.1182/blood-2005-08-3101.

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Abstract Multiple myeloma (MM) is characterized by the production of monoclonal immunoglobulin and is associated with suppressed uninvolved immunoglobulins and dysfunctional T-cell responses. The biologic basis of this dysfunction remains ill defined. Because T regulatory (Treg) cells play an important role in suppressing normal immune responses, we evaluated the potential role of Treg cells in immune dysfunction in MM. We observed a significant increase in CD4+CD25+ T cells in patients with monoclonal gammopathy of undetermined significance (MGUS) and in patients with MM compared with healthy donors (25% and 26%, respectively, vs 14%); however, Treg cells as measured by FOXP3 expression are significantly decreased in patients with MGUS and MM compared with healthy donors. Moreover, even when they are added in higher proportions, Treg cells in patients with MM and MGUS are unable to suppress anti-CD3–mediated T-cell proliferation. This decreased number and function of Treg cells in MGUS and in MM may account, at least in part, for the nonspecific increase in CD4+CD25+ T cells, thereby contributing to dysfunctional T-cell responses.

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Sutherland, Wayne H. F., Sylvia A. de Jong, and Robert J. Walker. "Effect of Dietary Cholesterol and Fat on Cell Cholesterol Transfer to Postprandial Plasma in Hyperlipidemic Men." Lipids 42, no. 10 (August 7, 2007): 901–11. http://dx.doi.org/10.1007/s11745-007-3101-1.

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Demirci, Selami, Ayşegül Doğan, Hüseyin Apdik, Emre Can Tuysuz, Sukru Gulluoglu, Omer Faruk Bayrak, and Fikrettin Şahin. "Cytoglobin inhibits migration through PI3K/AKT/mTOR pathway in fibroblast cells." Molecular and Cellular Biochemistry 437, no. 1-2 (June 15, 2017): 133–42. http://dx.doi.org/10.1007/s11010-017-3101-2.

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Micallef, Ivana, Patrick J. Stiff, John F. DiPersio, Richard Thomas Maziarz, John M. McCarty, Jennifer Angell, Gary Bridger, and Gary Calandra. "Successful Stem Cell Mobilization Rescue by AMD3100 (Plerixafor)+G-CSF for Patients Who Failed Primary Mobilization: Results from the Phase III (3101-NHL) Study." Blood 110, no. 11 (November 16, 2007): 602. http://dx.doi.org/10.1182/blood.v110.11.602.602.

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Abstract Background: AMD3100 (plerixafor)+G-CSF (A+G) was generally safe and more effective in mobilizing CD34+ hematopoietic stem cells compared to placebo+G-CSF (P+G) in a Phase III, multicenter, randomized, double-blind, placebo controlled study conducted in patients with non-Hodgkin’s lymphoma (NHL). In the intent-to-treat analysis, 78/148 (53%) patients in the P+G group and 20/150 (13%) patients in the A+G group failed to mobilize ≥ 2 x 106 CD34+ cells/kg, p<0.0001. Of these failure patients, 52 in the P+G group and 10 in the A+G group consented to enter into the rescue arm of the study. This abstract reports the outcomes of these rescue patients. Methods: Patients enrolled in the Phase III study who failed to mobilize ≥2 x 106 CD34+ cells/kg could enter into the rescue arm of the study and receive A+G. The patient’s treatment assignment in the study remained blinded. Following a rest period of ≥7 days, patients were given G (10 μg/kg/day) subcutaneously (SQ) for 4 days. In the evening around 10PM on Day 4, patients were given a dose of A (240 μg/kg SQ). On Day 5, all patients returned to clinic to receive a morning dose of G before apheresis. Patients continued to receive the evening dose of A followed by morning dose of G and apheresis the next day for up to a total of 4 aphereses or until ≥5 x 106 CD34+ cells/kg were collected. Pooled cells were allowed for transplantation. Results: After rescue therapy, 33/52 (63%) patients who previously failed P+G and 4/10 (40%) patients who previously failed A+G collected ≥2 x 106 CD34+ cells/kg. Seven of the 33 patients who previously failed with P+G collected ≥ 5 x 106 CD34+ cells/kg. Six of the ten A+G patients and 46/52 P+G patients were transplanted. Median time to PMN engraftment was Day 10 and Day 11 for the A+G and P+G groups, respectively. Median time to platelet engraftment was Day 22 and Day 20 for the A+G and P+G groups, respectively. One patient in the P+G group never had platelet counts > 50,000 and was counted as a failure to engraft, even though the patient was clinically stable through 6 months post-transplant. In the re-mobilized group, 9 patients died (2 patients were never transplanted and 7 patients had disease progression). Grafts were durable for ≥100 days in all 6 rescued A+G patients and all 41 rescued P+G patients who engrafted. The predominant adverse events were mild gastrointestinal effects (diarrhea, nausea, vomiting, and abdominal pain) and injection site reactions. There were no drug-related serious adverse events reported in these re-mobilized patients. Conclusions: The addition of AMD3100 to G-CSF successfully mobilized sufficient stem cells for transplant in 63% of NHL patients who previously failed mobilization with G-CSF alone. The high success rate is consistent with the Compassionate Use Protocol experience. AMD3100 was generally well tolerated. The 40% success rate in the patients who previously failed AMD3100+G-CSF suggests that re-mobilization with the same combination is a potentially useful strategy for similar patients.

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Yamasaki, Sho, Eri Ishikawa, Masayuki Kohno та Takashi Saito. "The quantity and duration of FcRγ signals determine mast cell degranulation and survival". Blood 103, № 8 (15 квітня 2004): 3093–101. http://dx.doi.org/10.1182/blood-2003-08-2944.

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Abstract Immunoglobulin E (IgE) bound to multivalent antigen (Ag) elicits mast cell degranulation but not survival; on the contrary, IgE in the absence of Ag (IgE(-Ag)) induces survival only but not degranulation. Although these distinct responses are mediated through the same receptor, FcϵRI, the molecular mechanism generating the divergence is largely unknown. We recently showed that the signals through FcRγ chain are essential for IgE(-Ag)–induced mast cell survival as well as IgE(+Ag)–induced degranulation. To determine whether the cellular output is regulated by the quantity of FcRγ signal, we expressed CD8/FcRγ chimeras (CD8/γ) in bone marrow–derived mast cells (BMMCs) from FcRγ-/- mice to manipulate the strength of FcRγ signals by anti-CD8 cross-linking. Cross-linking of CD8/γ induced mast cell survival and degranulation. Survival was induced by weaker stimulation than needed for degranulation in terms of anti-CD8 concentration and the valency of chimera. However, sustained extracellular signal-regulated kinase (Erk) activation seems to regulate survival even when the activation signal was strong enough to elicit degranulation. Generation of sustained Erk activation by active mitogen-activated protein kinase kinase (MEK) induced BMMC survival. These results suggest that the duration and the magnitude of FcRγ signals may determine mast cell survival and degranulation, respectively. (Blood. 2004;103:3093-3101)

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Delvino, P., F. Sardanelli, S. Monti, P. Cohen, X. Puéchal, C. Montecucco, L. Mouthon, L. Guillevin, and B. Terrier. "AB0467 REMISSION AND LOW DISEASE ACTIVITY STATE IN PATIENTS WITH GRANULOMATOSIS WITH POLYANGIITIS AND MICROSCOPIC POLYANGIITIS: PREVALENCE AND IMPACT ON DAMAGE ACCRUAL." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1531.1–1532. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3101.

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Background:Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) require glucocorticoids (GCs) and immunosuppressants (IS) to induce and maintain remission. At the era of highly active drugs and treat-to-target strategies, defining the goal to achieve in terms of remission could be beneficial for the long-term management.Objectives:To assess the impact of prolonged remission or low disease activity state (LDAS) in GPA and MPA patients and its relationship with damage accrual.Methods:Patients diagnosed with GPA and MPA, according to ACR criteria and/or Chapel Hill definitions, seen in two vasculitis centers and followed-up for ≥5 years were included. Disease activity was assessed by BVAS, and damage accrual by the VDI. Three levels of remission were defined: complete remission (CR): BVAS=0 and negative ANCA in GCs-free and IS-free patients; clinical remission off therapy: no disease activity and positive ANCA in GCs-free and IS-free patients; clinical remission on therapy: no disease activity in patients with low dose GCs (≤5 mg/d) and/or IS. LDAS was defined as 0<BVAS≤3 without major organ activity, no new disease activity, low-dose GCs (≤7.5 mg/day) and well-tolerated IS. We defined remission or LDAS as prolonged when lasting ≥2 consecutive years. The effect of prolonged remission and LDAS on damage accrual was evaluated.Table.Prevalence of vasculitic affection of respective arteries in patients with giant cell arteritis and polymyalgia rheumatica and patients with giant cell arteritis only.Affected arteryGroupPMR-GCA-group (n=27)GCA-group (n=18)UnilateralBilateralNoneUnilateralBilateralnoneAxillary artery9 (33%)12 (45%)6 (22%)5 (28%)7 (39%)6 (33%)Common superficial temporal artery3 (11%)21 (78%)3 (11%)5 (28%)13 (72%)0 (0%)Frontal branch6 (22%)17 (63%)4 (15%)3 (17%)11 (61%)4 (22%)Parietal branch5 (18%)21 (78%)1 (4%)3 (17%)13 (72%)2 (11%)Facial artery7 (26%)17 (63%)3 (11%)4 (22%)11 (61%)3 (17%)PMR-GCA-group: patients with diagnosis of giant cell arteritis and consecutive polymyalgia rheumaticaGCA-group: patients with diagnosis of giant cell arteritis onlyResults:167 patients were included: 128 (76.6%) GPA, mean age 51.0±16.7 years. At 5-years, mean VDI was 2.7±2.0, mainly because of AAV-related items (2.0±1.7) rather than treatment-related items (0.7±1.0). During the 5-year follow-up, 10 (6.0%) patients achieved prolonged CR, 6 (3.6%) prolonged clinical remission off therapy, 89 (53.3%) prolonged clinical remission on therapy, 42 (25.1%) prolonged LDAS and 20 (12.0%) never achieved LDAS. Damage accrual at 5-years in patients with prolonged CR, clinical remission off therapy, clinical remission on therapy, LDAS or those never achieved LDAS was 1.6±1.1, 1.8±1.7, 2.3±1.9, 3.8±2.0 and 3.3±2.0, respectively (P<0.0001). Damage was comparable between patients in prolonged remission off therapy and those in remission on therapy (P=0.3). In contrast, patients in prolonged LDAS or those never in LDAS had significantly more damage accrual (P<0.0001 and P=0.01, respectively) than those in prolonged remission off therapy. Eighty-one patients (49%) reached a VDI ≥3 at 5-years. The inability to achieve prolonged remission was associated with a VDI ≥3 at 5-years (OR 5.07, 95% CI 2.53-9.84, P<0.0001), and considering only prolonged CR or clinical remission off therapy did not had any benefit on damage accrual. In contrast, achieving prolonged LDAS had no benefit compared to spending no time in LDAS (P>0.99). Compared to patients achieving prolonged remission, those not able to achieve prolonged remission were younger (46±16.0 vs. 53.5±16.6, P=0.001), had more frequent GPA (P=0.0003), had more PR3-ANCA (P=0.006), had more ENT and lung involvement (P<0.0001 and P=0.036, respectively).Conclusion:Sixty percent of GPA and MPA patients achieved prolonged remission, which was associated with a better outcome in terms of damage accrual. In contrast, prolonged LDAS was associated with increased damage and was not a sufficient target to achieve in GPA and MPA.Disclosure of Interests: :None declared

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D'Souza, Anita, Francis K. Buadi, Martha Q. Lacy, Morie A. Gertz, Suzanne R. Hayman, Shaji Kumar, David Dingli, Steven R. Zeldenrust, and Angela Dispenzieri. "Relapse of POEMS Following Autologous Stem Cell Transplantation: A Single Center Experience." Blood 118, no. 21 (November 18, 2011): 3101. http://dx.doi.org/10.1182/blood.v118.21.3101.3101.

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Abstract Abstract 3101 The POEMS (polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes) syndrome is a rare paraneoplastic disorder secondary to a clonal plasma cell process. The most experience with successful outcomes in POEMS with disseminated disease has been with high dose chemotherapy followed by autologous stem cell transplantation (ASCT). However, the risk of relapse of POEMS following an ASCT or the outcome of the patients who relapse is not known. We therefore performed a retrospective review of POEMS patients who underwent ASCT at our center and subsequently relapsed or progressed. Over the past 12 years, 58 patients with POEMS underwent autologous stem cell transplantation at the Mayo Clinic, Rochester between Mar 18, 1999 and Jun 22, 2011. With a median follow up of 40 months (1–147 months), 12 patients have relapsed. The median time to relapse was 41 months. The 1, 2, and 5 year PFS rates were 98%, 94%, and 75%, respectively (Figure 1), and the 1, 2, and 5 year OS rates were 98%, 98%, and 94%. Of the 12 patients with documented relapse, 7 had baseline PET/CT scans all of which had FDG avid lesions. By 1 year, the FDG avidity had not resolved in 4 of these patients who then went on to either develop additional lesions or increasing SUV of existing lesions. Of the 12 patients with documented relapse, 8 had baseline VEGF measurements, and all but 1 had normalization by 1 year. The first sign of relapse was a clinical deterioration in 2, a rising M-protein in 3, and a rising plasma VEGF level in 5 patients. All of these patients had new or worsening of existing lesions on PET/CT scan (n= 9) or x-ray imaging (n= 3). The symptoms of clinical relapse included pain at the site of the lytic lesion and generalized pain with swelling. Of the patients who relapsed, 5 were treated with radiation therapy, 4 received lenalidomide or thalidomide, 2 had alkylator based therapy and 1 had bortezomib based therapy. One patient was treated with surgical resection of his hepatic plasmacytoma and 2 patients have been observed without needing definitive treatment as of yet. One patient also received anti-VEGF treatment with bevacizumab unsuccessfully after failing cyclophosphamide therapy. In this large cohort of POEMS patients treated with high dose chemotherapy and autologous stem cell transplantation in a single center, a relapse rate of 21% was noted. Not every patient who relapsed has been deemed to need further treatment, and most patients could be salvaged with chemotherapy or radiation. Only one patient died from relapsed POEMS following stem cell transplantation. Disclosures: No relevant conflicts of interest to declare.

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Johnson, Emhonta, Christopher S. Theisen, Keith R. Johnson, and Margaret J. Wheelock. "R-cadherin influences cell motility via Rho family GTPases. Vol. 279 (2004) 31041-31049." Journal of Biological Chemistry 279, no. 42 (October 2004): 44229–30. http://dx.doi.org/10.1016/s0021-9258(20)68100-5.

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van Heijst, Jeroen W. J., Izaskun Ceberio, Lauren B. Lipuma, Dane W. Samilo, Gloria D. Wasilewski, Anne Marie R. Gonzales, Jimmy L. Nieves, Marcel R. M. van den Brink, Miguel A. Perales, and Eric G. Pamer. "Quantitative assessment of T cell repertoire recovery after hematopoietic stem cell transplantation." Nature Medicine 19, no. 3 (February 24, 2013): 372–77. http://dx.doi.org/10.1038/nm.3100.

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Cubas, Rafael A., Joseph C. Mudd, Anne-Laure Savoye, Matthieu Perreau, Julien van Grevenynghe, Talibah Metcalf, Elizabeth Connick, et al. "Inadequate T follicular cell help impairs B cell immunity during HIV infection." Nature Medicine 19, no. 4 (March 10, 2013): 494–99. http://dx.doi.org/10.1038/nm.3109.

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Більше джерел

Дисертації з теми "3101 Biochemistry and cell biology"

Hodzic, Denis. "Effects of EF-24 and Cisplatin on Cancer, Renal, and Auditory Cells." TopSCHOLAR®, 2019. https://digitalcommons.wku.edu/theses/3110.

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Cisplatin is a chemotherapy drug effective against several forms of cancer, but can also cause serious side-effects, including nephrotoxicity and ototoxicity. Curcumin, a natural plant compound, can increase cisplatin’s anti-cancer activity and counteract cisplatin’s deleterious effect on the auditory and renal systems. Unfortunately, curcumin exhibits poor bioavailability, which has promoted interest in the development of synthetic curcumin analogs (curcuminoids) that are soluble, target cancer, and do not cause side effects. This study investigated whether the curcuminoid (3E,5E)-3,5-bis[(2-fluorophenyl) methylene]-4-piperidinone (EF-24) increases the anti-cancer effects of cisplatin against a human ovarian cancer cell line (A2780) and its cisplatin-resistant counterpart (A2780cis), while preventing cisplatin-mediated side effects in a human kidney cell line (HEK-293T) and a mouse auditory hybridoma cell line (HEI-OC1). The effect of cisplatin and EF-24 on cellular viability was measured using the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. The expression and activity of signal transduction proteins in several apoptotic pathways was measured using caspase luminescence assays. Reactive oxygen species (ROS) production was also measured using flow cytometry. Our data suggest that cisplatin and EF-24 are effective against ovarian cancer cell lines, but both compounds may also have adverse effects on auditory and renal cells. This project provides relevant information that may improve our understanding of how these compounds function in different tissues, facilitating improved cancer treatment and circumvention of side effects commonly associated with cisplatin treatment.

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Camacho, Diogo Mayo. "In silico cell biology and biochemistry: a systems biology approach." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/27960.

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In the post-"omic" era the analysis of high-throughput data is regarded as one of the major challenges faced by researchers. One focus of this data analysis is uncovering biological network topologies and dynamics. It is believed that this kind of research will allow the development of new mathematical models of biological systems as well as aid in the improvement of already existing ones. The work that is presented in this dissertation addresses the problem of the analysis of highly complex data sets with the aim of developing a methodology that will enable the reconstruction of a biological network from time series data through an iterative process. The first part of this dissertation relates to the analysis of existing methodologies that aim at inferring network structures from experimental data. This spans the use of statistical tools such as correlations analysis (presented in Chapter 2) to more complex mathematical frameworks (presented in Chapter 3). A novel methodology that focuses on the inference of biological networks from time series data by least squares fitting will then be introduced. Using a set of carefully designed inference rules one can gain important information about the system which can aid in the inference process. The application of the method to a data set from the response of the yeast Saccharomyces cerevisiae to cumene hydroperoxide is explored in Chapter 5. The results show that this method can be used to generate a coarse-level mathematical model of the biological system at hand. Possible developments of this method are discussed in Chapter 6.
Ph. D.

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Agüera-González, Sonia. "Cell biology on NKG2D ligands and NK cell recognition." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609348.

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Delorme, Marilyne. "Downregulation of ATRX disrupts cell proliferation and cell cycle progression." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27627.

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ATRX is a chromatin remodelling protein of the SNF2 family of chromatin remodelling proteins. Mutations in the ATRX gene have been shown to cause the ATR-X syndrome, an X-linked mental retardation disorder. ATRX is part of a chromatin-remodelling complex with Daxx that localizes to PML nuclear bodies or pericentromeric heterochromatin and is thought to regulate gene expression. In mice, Atrx inactivation results in embryonic lethality whereas conditional forebrain specific Atrx ablation showed impaired development and disorganization of the cortex. Furthermore, ATRX phosphorylation was shown to be cell cycle dependant, suggesting an important role for ATRX in cell cycle regulation. In this study we investigated the effects of ATRX downregulation in cell culture models, using siRNA transient transfection, a clone expressing an shRNA targeted to ATRX, and Atrxnull MEFs. ATRX downregulated cells showed reduced growth rates and cell cycle defects at the G1 and S phases of the cell cycle. Moreover, ATRX ablation was associated with an altered Rb phosphorylation status and decreased expression of the cyclin A and E2F-1 proteins. Taken together our results suggest that ATRX may play a significant role in cell cycle progression that is pertinent for proper development.

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Ye, Qing. "LIPASE-KINASE ASSOCIATIONS INVOLVING PLD2, JAK3 AND FES THAT UNDERLIE CANCER CELL PROLIFERATION AND INVASION." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1421939242.

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Chu, Wei. "Mouse Mast Cell Proteases: Induction, Molecular Cloning, and Characterization." Digital Commons @ East Tennessee State University, 1991. https://dc.etsu.edu/etd/2656.

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Tryptase, a mast cell-specific serine protease with trypsin-like specificity, has been identified in a mouse mast cell line (ABFTL-6) based on it's enzymatic activity, inhibition properties, and cross-reactivity to a human mast cell tryptase antibody. The effects of fibroblast-conditioned medium and sodium butyrate on ABFTL-6 mast cell differentiation and tryptase expression have been examined. ABFTL-6 mouse mast cells undergo phenotypic changes upon culturing in media supplemented with fibroblast-conditioned media at 50% or 1 mM sodium butyrate. The induced cells increased in size, had larger and more metachromatic cytoplasmic granules, and increased their total cellular protein about four-fold. Tryptase activity increased 13- and 6-fold upon fibroblast-conditioned media and butyrate induction, respectively. However, tryptase antigen levels increased dramatically from 2.3 $\mu$g/10$\sp6$ uninduced cells to 125 (54-fold) and 75 (33-fold) $\mu$g/10$\sp6$ cells induced with fibroblast-conditioned media or butyrate, respectively. A cDNA library was constructed in $\lambda$gt10 from ABFTL-6 cell poly(A)$\sp+$ RNA, and screened with dog mast cell tryptase and rat mast cell chymase cDNAs. Clones encoding two distinct tryptases (mouse tryptases I and II), a chymase (mouse chymase I) and a novel carboxyl terminal chymase (mouse chymase II) were isolated and sequenced. Mouse tryptases I and II have 75% and 70% sequence identity at the nucleotide and amino acid levels, respectively. The deduced amino acid sequence for the mature active enzyme for each mouse tryptase contains 245 residues and all the characteristics of a serine protease. Asp is found in the substrate binding pockets, consistent with a trypsin-like specificity for Arg-X and Lys-X bonds. It is predicted that tryptases are synthesized with prepropeptides, requiring signal peptidase processing and removal of a three amino acid propeptide for activation. Mouse chymase I consists of a 226 amino acid catalytic portion and a 21 amino acid preprosequence. An Asn occurs in the substrate binding pocket, a feature that has not been observed in any other serine protease.

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Bainor, Anthony J. "Elucidating the Role of SIN3B as a Regulator of Cell Cycle Exit." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10604607.

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Progression through the mammalian cell cycle is a tightly regulated process that allows cells to replicate their genomes and divide properly. In growth factor-deprived conditions or in response to stress, the cell will exit the cell cycle either reversibly through quiescence, or permanently via senescence. Studies have shown that the SIN3 family of proteins plays a crucial role in these cell cycle exit processes. SIN3 proteins are highly conserved, and exist in mammals as two family members: SIN3A and SIN3B, which function as flexible scaffolding proteins to assemble co-repressor complexes. Our laboratory has recently implicated SIN3B as a critical mediator of each of these cell cycle exit processes. However, its mechanism of action and the consequences of its disruption pertaining to cancer progression have not been comprehensively elucidated. Here we demonstrate that SIN3B is required for the induction of senescence in a mouse model of prostate cancer, and thus prevents the progression to aggressive and invasive carcinoma. In addition, through interaction analysis, we uncovered a novel and robust association between SIN3B and the DREAM complex. The DREAM complex, comprised of p107/p130, E2F4/5, DP1 and the MuvB core complex, is responsible for the repression of hundreds of cell cycle-related transcripts during quiescence. We determined that the deletion of SIN3B resulted in the derepression of DREAM target genes during quiescence, but was not sufficient to allow quiescent cells to resume proliferation. However, the ectopic expression of APC/C^CDH1 inhibitor EMI1 was sufficient for SIN3B deleted cells, but not wild-type cells, to reenter the cell cycle. These studies demonstrate a critical role for SIN3B in the senescence and quiescence programs, and provide important mechanistic insight into the molecular pathways that exquisitely regulate cell cycle exit.

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Reimer, Michael. "Characterization of IQGAP1 Protein in Areas of Cell Retraction." Thesis, Southern Illinois University at Edwardsville, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1582876.

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IQGAP1 interacts with numerous binding partners through a calponin homology domain (CHD), a WW motif, IQ repeats, a Ras GAP related domain (GRD), and a conserved C-terminal (CT) domain. Among various biological and cellular functions, IQGAP1 plays a role in cell-matrix interactions and actin cytoskeleton dynamics in membrane ruffling and lamellipodium protrusion. Phosphorylation in the CT domain regulates intramolecular interaction and IQGAP1 cellular activity. In a recent study, we discovered that IQGAP1 surprisingly localizes to actively retracting edges, instead of protruding areas, in B16F10 mouse melanoma cells and some other cells types. In these current studies we examined localization of IQGAP1 mutants to retracting versus protruding areas in phorbol ester-stimulated B16F10 cells. Cells were co-transfected with GFP-IQGAP1 full length (GFP-IQGAP1-FL), as an internal control, and one of five Myc-tagged IQGAP1 constructs (FL, CA, ΔCHD, ΔGRD or ΔCT). The cotransfected cells were plated onto laminin for 30 minutes, stained with anti-Myc and anti-WAVE2 antibodies, and normalized fluorescence measurements were made in retracting and protruding areas. Retracting cell areas were defined as GFP-IQGAP1-FL positive and WAVE2 negative, while protruding cell areas were defined as GFP-IQGAP1-FL negative and WAVE2 positive. In retracting areas there were large decreases in both ΔGRD and ΔCT localization, a slight decrease in ΔCHD localization, and normal localization of the CA mutant. In areas of cell protrusion there were large increases in both ΔGRD and ΔCT localization, and normal localization of ΔCHD and CA mutants. These results indicate that two domains, GRD and CT, are essential for normal localization of IQGAP1 to retracting cell areas. Furthermore, our results suggest a model in which IQGAP1 in the areas of cell retraction is in the open, phosphorylated, conformation. Additionally we investigated the knockdown of IQGAP1 in B16F10 cells by means of actin images. Cells were exposed to the lentil virus which contained short hairpin Ribonucleic acid (shRNA) that would silence IQGAP1. Two controls were used in the experiment, untransfected B16F10 cells and B16F10 cells which were exposed to the lentil virus without any shRNA. We found that the knockdown cells were in general much more compact and that they did not polarize. Surface stiffness was investigated in the effect it would have on B16F10 cells. Polyacrylamide gels were made and cross-linked using sulfo-SANPAH. Laminin was added to the cross-linked gels and B16F10 cells were placed on top of the laminin coated hydrogels. Investigation of the cells by means of actin images revealed that surface stiffness had an effect on cell morphology. The 1 kPa surfaces did not allow for spreading of the cells, while the surfaces greater than 100 kPa exhibited normal cell behavior.

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Hussey, P. J. "Studies on the molecular and cell biology of plant tubulin." Thesis, University of Kent, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376791.

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Upcher, William R. "Biochemical studies of the cohesin complex." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:e9a77a9c-40a5-466d-a894-c7fefeddef52.

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The accurate inheritance of genetic material depends upon the establishment and maintenance of sister chromatid cohesion. Replicated chromosomes are topologically encircled by the large, tripartite protein complex cohesin, allowing bi-orientation in mitosis. To entrap and reversibly dissociate from DNA, the annular complex structure must be disrupted at either the hinge domain between Smc1 and Smc3, or the interfaces created by the kleisin subunit Scc1 bridging the two ABC-like ATPase domains. The aim of this work was to characterise the cohesin complex loading and releasing mechanisms by examining the biochemical requirements for these processes. Although the identity of a chromosomal cofactor could not be assigned, the loading reaction was found to necessitate engagement of ATPase domains in an ATP-dependent manner. Notions of allosteric modulation of ATP binding and NBD engagement by acetylation were discredited. Likewise, a direct and stable physical association of hinge domains with NBDs was shown to be an unlikely conformational intermediate in a reaction thought to promote hinge opening for loading of cohesin onto DNA. The Smc3-Scc1 kleisin interface might be exploited during the opposing process of release of cohesin from DNA. Therefore, a novel protein- protein cross-linking system was adapted for use in S. cerevisiae, with a view to (1) confirming the well-founded role of hinge dissociation in topological entrapment, and (2) validating the Smc3- Scc1 interface as the recently conjectured exit gate. Despite promising preliminary kinetics in vitro, the SpyTag-SpyCatcher system was considerably less efficient in vivo. It was thus deemed unsuitable in its current format for investigating the process of interface dissociation in live cells. Finally, the large, cohesin complex-associated HEAT repeat protein Pds5 has been either speculated or shown to participate in all of the aforementioned processes, potentially modulating the hinge and Smc-kleisin interfaces. Acting as a regulatory node in cohesin function, it was pursued as an informative target for structural studies. Although no diffractive material could be obtained, Pds5 was confirmed to bind a short, N-terminal sequence of Scc1 and was in turn bound at its N- terminus by Wapl. Together, these findings contribute to defining the structures and states of the cohesin complex.

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Книги з теми "3101 Biochemistry and cell biology"

Lyn, Shepherd, and Allan Richard 1954-, eds. Cell biology & biochemistry. Hamilton, N.Z: Biozone International, 2006.

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Estes, James E. Actin: Biophysics, Biochemistry, and Cell Biology. Boston, MA: Springer US, 1994.

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Schwartzbach, Steven D., and Shigeru Shigeoka, eds. Euglena: Biochemistry, Cell and Molecular Biology. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54910-1.

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Kreitzer, Geri, Fanny Jaulin, and Cedric Espenel. Cell biology assays: Proteins. Amsterdam: Elsevier/Academic Press, 2010.

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A, Cogoli, ed. Cell biology and biotechnology in space. Amsterdam: Elsevier, 2002.

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Bruce, Alberts, ed. Essential cell biology. 3rd ed. New York: Garland Science, 2009.

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Bruce, Alberts, ed. Essential cell biology. 2nd ed. New York, NY: Garland Science Pub., 2004.

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Bruce, Alberts, ed. Essential cell biology. Abingdon: Garland Science Pub., 1997.

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Rosann, Tung, ed. Essential cell biology test bank. New York: Garland Pub., 1997.

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An-Ping, Zeng, and SpringerLink (Online service), eds. Genomics and Systems Biology of Mammalian Cell Culture. 2nd ed. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012.

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Частини книг з теми "3101 Biochemistry and cell biology"

Rodríguez, E. M. "Cell Biology and Biochemistry." In The Subcommissural Organ, 309–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78013-4_32.

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Severs, Nicholas J. "Cholesterol Cytochemistry in Cell Biology and Disease." In Subcellular Biochemistry, 477–505. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5901-6_16.

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Stewart, A. K., I. D. Dubé, and R. G. Hawley. "Gene Marking and the Biology of Hematopoietic Cell Transfer in Human Clinical Trials." In Blood Cell Biochemistry, 243–68. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4889-8_9.

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Roncero, Cesar, Alberto Sanchez-Diaz, and M. Henar Valdivieso. "9 Chitin Synthesis and Fungal Cell Morphogenesis." In Biochemistry and Molecular Biology, 167–90. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27790-5_9.

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Lee, Mark J., and Donald C. Sheppard. "8 The Cell Wall Polysaccharides of Aspergillus fumigatus." In Biochemistry and Molecular Biology, 147–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27790-5_8.

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Hussain, Mahboob Ul. "General Cell Biology of Connexins." In SpringerBriefs in Biochemistry and Molecular Biology, 7–9. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1919-4_4.

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Chan, Edmond Y. W., Robert Köchl, and Sharon A. Tooze. "Cell Biology and Biochemistry of Autophagy." In Autophagy in Immunity and Infection, 19–53. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/352760880x.ch2.

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Suzuki, K., G. van Echten-Deckert, A. Klein, and K. Sandhoff. "Glycosphingolipids and sphingolipid activator proteins: Cell biology, biochemistry and molecular genetics." In Biochemistry of Cell Membranes, 137–49. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9057-1_10.

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Harrison, Michael A., and Steven P. Muench. "The Vacuolar ATPase – A Nano-scale Motor That Drives Cell Biology." In Subcellular Biochemistry, 409–59. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7757-9_14.

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de Oliveira Buanafina, Marcia Maria, and Daniel J. Cosgrove. "Cell Walls: Structure and Biogenesis." In Sugarcane: Physiology, Biochemistry, and Functional Biology, 307–29. Chichester, UK: John Wiley & Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118771280.ch13.

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Тези доповідей конференцій з теми "3101 Biochemistry and cell biology"

Schleuning, W. D. "THE BIOCHEMISTRY AND CELL BIOLOGY OF SINGLE CHAIN UROKINASE TYPE PLASMINOGEN ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642956.

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Urokinase was discovered in the late nineteenth century, as an enzymatic principle in urine, that initiates the dissolution of blood clots. The basis of this phenomenon was recognized more than fifty years ago as the activation of plasminogen, the precursor of a tryptic protease, then known as profibrinolysin. Despite this long history, detailed data on the biochemistry of plasminogen activation have only become available recently. Urokinase (now designated urokinase-type plasminogen activator : u-PA) is synthesized and secreted as a single chain polypeptide (Mr-: 53,000) by many cell types. Single chain u-PA (scu-PA) is with equal justification called prourokinase (pro-u-PA), notwithstanding its low catalytic activity for synthetic peptide substrates and plasminogen, as most proenzymes of proteases display a certain degree of activity. The structure of pro-u-PA has been elucidated by protein and cDNA sequencing. It consists of three domains, exhibiting characteristic homology to other proteins: a serine protease domain, homologous to trypsin, chymotrypsin and elastase; a kringle domain, likewise found in prothrombin, plasminogen, tissue-type plasminogen activator (t-PA) and Factor XII; and an epidermal growth factor (EGF)-like domain, found in many other proteins, including certain clotting factors. Pro-u-PA is activated by the cleavage of its LYS158-Ile159 h1 bY either plasmin or kallikrein. This cleavage leads to a high increase of Kcat values with respect to both plasminogen and synthetic peptide substrates, but apparently to a reduction of its affinity to plasminogen. Thrartoin inactivates pro-u-PA irreversibly by the cleavage of the Arg156-Phe157 bond. U-PA but not pro-u-PA rapidly forms ccnplexes with plasminogen activator inhibitors (PAI)-l and PAI-2: second order rate constants Kass are respectively > 107 and 0.9xl06 (M-11sec-1). Unknown enzymes process pro-u-PA and u-PA to low molecular weight (LMW) pro-u-PA and LMW u-PA (Mr: 33,000) by cutting off a fragment consisting of the kr ingle and the EGF—like region. Pro—u—PA mediated plasminogen activation is fibrin dependent in vivo, and to a certain degree in vitro. Hie biochemical basis of this fibrin specificity is at present uncertain, although there are reports indicating that it may require polyvalent cations. Through its EGF-like region HMW pro-u-PA and HMW u-PA are capable of binding to specific membrane protein receptors which are found on many cells. Thus, u-PA activity may be restricted to the cell surface. According to a recent report, binding of u—PA to the receptor may also mediate signal transduction in auto- or paracrine growth control. In cells permissive for the respective pathways, pro-u-PA gene transcription is stimulated by mechanisms of signal transduction, that include the cAMP, the tyrosine specific kinase and the protein kinase C dependent pathways. Glucocorticoid hormones downregulate pro-u-PA gene transcription in cells where the gene is canstitutively expressed. Although different cells vary greatly in their response to agents that stimulate urokinase biosynthesis, growth factors and other mitogens are in many cases effective inducers. Significantly elevated levels of u-PA are also found in many malignant tissues. These findings and many others suggest that plasminogen activation by u-PA provides localized extracellular matrix degradation which is required for invasive growth, cell migration and other forms of tissue remodelling. Fibrin represents in this view only a variant of an extracellular matrix, which is provided through the clotting system in the case of an emergency.

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Young, Paul W. "Student-produced video of role-plays on topics in cell biology and biochemistry: A novel undergraduate group work exercise." In Learning Connections 2019: Spaces, People, Practice. University College Cork||National Forum for the Enhancement of Teaching and Learning in Higher Education, 2019. http://dx.doi.org/10.33178/lc2019.15.

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Group work or cooperative learning is a form of active learning that has potential benefits that extend beyond just being an alternative or improved way of learning course material. For example, Shimazoe and Aldrich (2010) identified six proposed benefits of active learning to students, namely (1) promoting deep learning, (2) helping students earn higher grades, (3) teaching social skills & civic values, (4) teaching higher order thinking skills, (5) promoting personal growth and (6) developing positive attitudes toward autonomous learning. There is evidence for the effectiveness of role-plays both in achieving learning outcomes (Azman, Musa, & Mydin, 2018; Craciun, 2010; Latif, Mumtaz, Mumtaz, & Hussain, 2018; McSharry & Jones, 2000; Yang, Kim, & Noh, 2010), but also in developing desirable graduate attributes such as teamwork, communication and problem solving skills [4]. The importance of such skills is widely touted by employers of science graduates, sometimes more so than discipline-specific knowledge, arguing in favour of the incorporation of role-plays and other forms of cooperative learning into undergraduate science curricula. Role-playing is probably not as widely used in the physical and life sciences as it is in other academic disciplines. In science the most obvious role-play scenarios in which students play the roles of people might be in examining historical figures at the centre of famous scientific discoveries or debates (Odegaard, 2003). In addition, role-plays fit well at the interface between science and other discipline when exploring ethical, legal or commercial implications of scientific discoveries(Chuck, 2011). However, to apply role-play to core topics in science or mathematics the roles that must be played are not those of people but rather of things like particles, forces, elements, atoms, numbers, laws, equations, molecules, cells, organs and so on. The learning scenarios for science-based roleplays in which the characters represented are not people are less obvious, probably explaining why the use of role-plays in science education is less common. Nevertheless, focusing on the life sciences, role-plays in which the characters are organelles in a cell or enzymes involved in fundamental cellular processes like DNA replication, RNA transcription and protein translation have been described for example (Cherif, Siuda, Dianne M. Jedlicka, & Movahedzadeh, 2016; Takemura & Kurabayashi, 2014). The communication of discipline-specific templates and successful models for the application of role-playing in science education is likely to encourage their wider adoption. Here I describe a videoed group role-play assignment that has been developed over a ten-year period of reflective teaching practice. I suggest that this model of videoed group role-plays is a useful cooperative learning format that will allow learners to apply their varied creativity and talents to exploring and explaining diverse scientific topics while simultaneously developing their teamwork skills.

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LeDuc, Philip. "Linking Molecular to Cellular Biomechanics With Nano- and Micro-Technology." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43987.

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The link between mechanics and biochemistry has been implicated in a myriad of scientific and medical problem, from orthopedics and cardiovascular medicine, to cell motility and division, to signal transduction and gene expression. Most of these studies have been focused on organ-level issues, yet cellular and molecular level research has become essential over the last decade in this field thanks to the revolutionary developments in genetics, molecular biology, fabrication processes, and biotechnology. Developing the link between molecular and cellular biomechanics through subcellular studies can help uncover the complex interactions requisite for understanding higher order macroscopic behavior. Here, we will explore the link between molecular and cellular research through novel systems of nano- and micro-technology. In this, I will discuss novel technologies that we have developed and are utilizing, which include magnetic needles, three-dimension cell stretching systems, and microfluidics to examine the link between mechanics and biochemistry (including structural regulation through the cytoskeleton). By combining these novel approaches between engineering and biology, this multidisciplinary research can make a tremendous impact on the studies of human health and diseases through advances in fields such as proteomics, tissue engineering, and medical diagnostics.

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Wechsler, Marissa E., Courtney M. Creecy, Christine F. O’Neill, and Rena Bizios. "Effects of Electrical Stimulation on Select Functions of Bone Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80367.

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The present in vitro study was motivated by scientific literature reports that show enhanced healing of bone fractures in experimental animals in response to electrical stimulation. The underlying cellular- and molecular level mechanisms responsible for new bone formation, however, were not studied at that time. Since then, advances in cell biology, biochemistry and biomedical engineering provided knowledge, models, and instrumentation to investigate these unanswered questions.

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Kaksis, Aris, Agnese Brangule, and Mihails Halitovs. "AN APPROACH TO TEACHING MEDICAL CHEMISTRY THAT HIGHLIGHTS INTERDISCIPLINARY NATURE OF SCIENCE." In 1st International Baltic Symposium on Science and Technology Education. Scientia Socialis Ltd., 2015. http://dx.doi.org/10.33225/balticste/2015.54.

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Thermodynamics is a branch of physics that deals with questions concerning energies and work of a system. It is one of the key topics for understanding processes in the universe as well as any separate system like a gas mixture or a single cell in a biological system. Thermodynamics is included in the university curriculum for engineering, chemistry and physics students as well as medical student curriculum. This paper outlines the problems faced by first year medical students learning thermodynamics at Riga Stradinš University. We describe a medically relevant context based approach to teaching that demonstrates the interdisciplinary nature of medical chemistry, molecular biology and biochemistry. Our method provides a model in which disciplinary barriers are diminished and increased effectiveness of teaching is achieved. Key words: interdisciplinary teaching, medical chemistry, thermodynamics, teaching and learning thermodynamics.

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Raykin, Julia, Alexander Rachev, Michael Zaucha, and Rudolph L. Gleason. "A Combined Theoretical-Experimental Paradigm for Studying Mechanical Conditioning of Tissue Engineered Arteries." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192746.

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There is a great unmet clinical need to develop small diameter tissue engineered blood vessels (TEBV) with low thrombogenicity and immune response, suitable mechanical properties, and a capacity to remodel to their environment [2, 3]. Development of a clinically useful small diameter TEBV will surely rely on techniques from a wide variety of disciplines, ranging from molecular and cell biology and biochemistry to material science and biomechanics. With regard to the latter, biomechanical stimuli, such as cyclic strain, have been shown to stimulate remodeling of collagen gel-derived TEBVs to greatly improve their mechanical behavior [5]. In native blood vessels, remodeling mechanisms appear to be aimed towards maintaining the local, 3-D mechanical environment (i.e., the local stresses or strains). It is becoming increasingly obvious that tissue engineered constructs also adapt to altered mechanical loading, and specific combinations of multidirectional loads appear to have a synergistic effect on the remodeling. Tissue engineered heart valve constructs exposed to cyclic flexure and shear stress, for example, exhibit a five-fold increase in production of extracellular matrix (ECM) constituents compared to constructs exposed to cyclic flexure or shear stress alone [1]. A critical gap remains, however, in understanding the role of both unidirectional and multidirectional loading on TEBV remodeling. Towards this end, we have developed theoretical and experimental frameworks to study remodeling of collagen and fibrin gel-derived TEBVs.

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Souchelnytskyi, Serhiy. "Systemic properties of Carcinogenesis: Lessons from studies on the Earth and in the Space." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0118.

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proteins and genes act in coordinated ways, and their relations are visualized as networks. Networks are more accurate descriptions of cancer regulatory mechanisms, in comparison to lists of oncogenes and tumor suppressors. To extract essential regulators (nodes) and connections (edges), interrogations of these networks are performed, e.g. cancer cells are subjected to different treatments. Interrogations force cancer cells to engage nodes and edges essential for maintaining cancer properties, i.e. drivers, and nonessential followers. The challenge is to discriminate which of the mechanisms drive tumorigenesis, and which are followers. Interrogation of cancer cells under variable g-forces is the treatment to which cancer cells are not normally exposed. Therefore, low (weightlessness) and high (acceleration) g-forces may trigger responses, which may differ in part of followers from responses on the Earth, but still engage carcinogenesis-essential drivers nodes and edges. Methodology: Experimental interrogation of human cancer cells to generate carcinogenesis-related regulatory networks was performed by using proteomics, cell biology, biochemistry, immunohistochemistry and bioinformatics tools. We used also reported datasets deposited in various databases. These networks were analyzed with algorithms to extract drivers of carcinogenesis. Results: Systemic analysis of human breast carcinogenesis has shown mechanisms of engagement of all known cancer hallmarks. Moreover, novel hallmarks have emerged, e.g. involvement of mechanisms of virus-cell interaction and RNA/miR processing. The breast cancer networks are rich, with >6,000 involved proteins and genes. The richness of the networks may explain many clinical observations, e.g. personalized response to treatments. Systemic analysis highlighted novel opportunities for treatment of cancer, by identifying key nodes of known and novel hallmark mechanisms. Systemic properties of the cancer network provides an opportunity to study compensatory mechanisms. These compensatory mechanisms frequently contribute to development of resistance to treatment. These mechanisms will be discussed. Cancer cells are not “wired” to function in weightlessness. The cells would have to adapt. This adaptation will include preserving mechanisms driving carcinogenesis, in addition to the space-only-related adaptation. Key carcinogenesis regulators in the space would be the same as on the Earth, while “passenger”-mechanisms would differ. Systems biology allows integration of a space- and the Earth-data, and would extract key regulators, and, subsequently lead to better diagnostic. Conclusion: Systemic analysis of carcinogenesis studies with different ways of interrogation delivered better diagnostic and novel modalities of treatment.

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