Готові списки джерел за темами / Ba93

Добірка наукової літератури з теми "Ba93"

Автор: Grafiati
Опубліковано: 27 липня 2024
Оновлено: 28 липня 2024

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Статті в журналах з теми "Ba93"

1

Flórez, Paola, Emanuela Di Martino, and Laís V. Ramalho. "Early Miocene coral reef-associated bryozoans from Colombia. Part I: Cyclostomata, “Anasca” and Cribrilinoidea Cheilostomata." Journal of Paleontology 95, no. 4 (March 16, 2021): 694–719. http://dx.doi.org/10.1017/jpa.2021.5.

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AbstractThis is the first of two comprehensive taxonomic works on the early Miocene (ca. 23–20 Ma) bryozoan fauna associated with coral reefs from the Siamaná Formation, in the remote region of Cocinetas Basin in the La Guajira Peninsula, northern Colombia, southern Caribbean. Fifteen bryozoan species in 11 families are described, comprising two cyclostomes and 13 cheilostomes. Two cheilostome genera and seven species are new: Antropora guajirensis n. sp., Calpensia caribensis n. sp., Atoichos magnus n. gen. n. sp., Gymnophorella hadra n. gen. n. sp., Cribrilaria multicostata n. sp., Cribrilaria nixor n. sp., and Figularia bragai n. sp. Eight species are identified only at genus level and remain in open nomenclature. Of the species found, 27% have erect colonies and 73% encrusting colonies. Both types contributed to the reef framework and produced sediment. The observed bryozoan diversity was higher in the barrier reefs than in the lagoonal patch reefs.UUID: http://zoobank.org/5c8468ef-31b0-4e7e-ba93-60a2e2f30b76.
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2

Gronostajski, Z. J. "Model describing the characteristic values of flow stress and strain of brass M63 and aluminium bronze BA93." Journal of Materials Processing Technology 78, no. 1-3 (June 1998): 84–89. http://dx.doi.org/10.1016/s0924-0136(97)00467-6.

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3

Dalimunthe, Cici Indriani, Radite Tistama, and Elia Wike Wijayanti Wijaya. "UJI BAKTERI ANTAGONIS UNTUK MENGENDALIKAN PENYAKIT MOULDY ROT (Ceratocystis fimbriata) DI LABORATORIUM." Jurnal Agro Estate 5, no. 1 (June 14, 2021): 39–48. http://dx.doi.org/10.47199/jae.v5i1.78.

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Анотація:
Ceratocystis fimbriata menyebabkan penyakit pada bidang sadap tanaman karet (Hevea brasiliensis), yang menyebabkan jamur abu-abu atau busuk pada panel sadap yang mempengaruhi hasil lateks. Tujuan penelitian adalah untuk memperoleh bakteri antagonis yang dapat menghambat pertumbuhan penyakit mouldy rot (Ceratocystis fimbriata) pada skala laboratorium. Penelitian ini menggunakan rancangan acak lengkap non-faktorial yang terdiri dari sepuluh perlakuan dan tiga ulangan. Bakteri Antagonis yang digunakan adalah BA1, BA3, BA4, BA5, BA6, BA7, BA8, BA9, dan BA10. Isolat bakteri diambil dari hasil isolasi kulit yang dipulihkan dan kulit tanaman karet perawan. Hasil penelitian menunjukkan bahwa isolat bakteri yang dapat menghambat pertumbuhan patogen sekitar > 80% adalah BA1, BA4, BA5, BA9, dan BA1. Isolat BA2, BA3, BA6, BA7, dan BA8 dapat menghambat pertumbuhan patogen jamur sekitar 40% hingga <80%. Isolat BA10 memiliki persentase penghambatan tinggi sekitar 92,84%. Pengujian lebih lanjut perlu dilakukan pada skala lapangan untuk menentukan efektivitasnya sebagai kontrol biologis penyakit mouldy rot.
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4

ROCH, Anne-Marie, Gerard QUASH, Yvonne MICHAL, Jacqueline CHANTEPIE, Bernard CHANTEGREL, Christian DESHAYES, Alain DOUTHEAU, and Jacqueline MARVEL. "Altered methional homoeostasis is associated with decreased apoptosis in BAF3 bcl2 murine lymphoid cells." Biochemical Journal 313, no. 3 (February 1, 1996): 973–81. http://dx.doi.org/10.1042/bj3130973.

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Анотація:
Methional is a potent inducer of apoptosis in an interleukin 3-dependent murine lymphoid cell line BAF3 b0 when it is added to the culture medium. In these cells transfected with the bcl2 gene, BAF3 bcl2, the apoptotic-inducing activity of methional is dramatically reduced. The addition of disulfiram (an inhibitor of aldehyde dehydrogenase) in order to reduce methional oxidation brought about an increase in apoptosis in BAF3 b0 but not in BAF3 bcl2 cells. In contrast, the addition of quercetin (an inhibitor of aldehyde reductase) in an attempt to diminish methional reduction increased apoptosis in both BAF3 b0 and BAF3 bcl2 cells. The extent of DNA fragmentation in BAF3 bcl2 cells approached that in BAF3 b0 cells in the presence of quercetin and exogenous methional, suggesting a defect in methional biosynthesis in BAF3 bcl2 cells. Direct evidence for this was obtained by measuring labelled methional in cells incubated with the sodium salt of [U-14C]4-methylthio-2-oxobutanoic acid (MTOB), the precursor of methional. The 80% decrease in labelled methional in BAF3 bcl2 compared with BAF3 b0 cells was accompanied by a concomitant rise in the transamination of [14C]MTOB to [14C]methionine in BAF3 bcl2 cells. Inhibition of the transaminase, however, by a synthetic transition-state-type compound, pyridoxal-L-methionine ethyl ester, induced apoptosis in BAF3 b0 but not in BAF3 bcl2 cells, confirming that the defect in BAF3 bcl2 cells was not in the transaminase itself but rather in the oxidative decarboxylation step MTOB →methional. In addition, no evidence was obtained for the synthesis of [14C]malondialdehyde from [14C]methional in BAF3 bcl2 cells. As these cells show no deficiency in their content of reactive oxygen species compared with that of BAF3 b0 cells, they may possess some other defect in the β-hydroxylase enzyme system itself.
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5

Hiebel, Christof, Elisabeth Stürner, Meike Hoffmeister, Georg Tascher, Mario Schwarz, Heike Nagel, Christian Behrends, Christian Münch, and Christian Behl. "BAG3 Proteomic Signature under Proteostasis Stress." Cells 9, no. 11 (November 4, 2020): 2416. http://dx.doi.org/10.3390/cells9112416.

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Анотація:
The multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3) represents a key player in the quality control of the cellular proteostasis network. In response to stress, BAG3 specifically targets aggregation-prone proteins to the perinuclear aggresome and promotes their degradation via BAG3-mediated selective macroautophagy. To adapt cellular homeostasis to stress, BAG3 modulates and functions in various cellular processes and signaling pathways. Noteworthy, dysfunction and deregulation of BAG3 and its pathway are pathophysiologically linked to myopathies, cancer, and neurodegenerative disorders. Here, we report a BAG3 proteomic signature under proteostasis stress. To elucidate the dynamic and multifunctional action of BAG3 in response to stress, we established BAG3 interactomes under basal and proteostasis stress conditions by employing affinity purification combined with quantitative mass spectrometry. In addition to the identification of novel potential BAG3 interactors, we defined proteins whose interaction with BAG3 was altered upon stress. By functional annotation and protein-protein interaction enrichment analysis of the identified potential BAG3 interactors, we confirmed the multifunctionality of BAG3 and highlighted its crucial role in diverse cellular signaling pathways and processes, ensuring cellular proteostasis and cell viability. These include protein folding and degradation, gene expression, cytoskeleton dynamics (including cell cycle and transport), as well as granulostasis, in particular.
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6

Liu, Yubo, Renjie Xu, Jinfu Xu, Tiantian Wu, and Xiangxin Zhang. "BAG3 regulates bone marrow mesenchymal stem cell proliferation by targeting INTS7." PeerJ 11 (August 9, 2023): e15828. http://dx.doi.org/10.7717/peerj.15828.

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Анотація:
Background BAG3 is an essential regulator of cell survival and has been investigated in the context of heart disease and cancer. Our previous study used immunoprecipitation-liquid chromatography-tandem mass spectrometry to show that BAG3 might directly interact with INTS7 and regulate bone marrow mesenchymal stem cell (BMMSCs) proliferation. However, whether BAG3 bound INTS7 directly and how it regulated BMMSCs expansion was unclear. Methods BAG3 expression was detected by quantitative real-time PCR in BMMSCs after siRNA-mediated BAG3 knockdown. BMMSC proliferation was determined using the CCK-8 and colony formation assays. The transwell migration, flow cytometry and TUNEL assays were performed to measure BMMSC migration, cell cycle and apoptosis, respectively. Moreover, co-immunoprecipitation, protein half-life assay and western blotting analyses were used to determine the regulatory mechanism underlying the BAG3-mediated increase in BMMSC proliferation. Results The results showed that knocking down BAG3 in BMMSCs markedly decreased their proliferative activity, colony formation and migratory capacity, and induced cell apoptosis as well as cell cycle arrest. Meanwhile, overexpression of BAG3 had the opposite effect. Bioinformatics and BAG3-INTS7 co-immunoprecipitation analyses revealed that BAG3 directly interacted with INTS7. Moreover, the downregulation of BAG3 inhibited the expression of INTS7 and promoted its ubiquitination. We also observed that BAG3 knockdown increased the levels of reactive oxygen species and the extent of DNA damage in BMMSCs. Notably, the upregulation of INTS7 or the addition of an antioxidant scavenger could rescue the BMMSC phenotype induced by BAG3 downregulation. Conclusions BAG3 directly interacts with INTS7 and promotes BMMSC expansion by reducing oxidative stress.
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7

Lee, Jae Chang, Sung Ae Koh, Kyung Hee Lee, and Jae-Ryong Kim. "BAG3 contributes to HGF-mediated cell proliferation, migration, and invasion via the Egr1 pathway in gastric cancer." Tumori Journal 105, no. 1 (December 4, 2018): 63–75. http://dx.doi.org/10.1177/0300891618811274.

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Анотація:
Introduction: Bcl2-associated athanogene 3 (BAG3) is elevated in several types of cancers. However, the role of BAG3 in progression of gastric cancer is unknown. Therefore, the present study aims to find out the role of BAG3 in hepatocyte growth factor (HGF)–mediated tumor progression and the molecular mechanisms by which HGF regulates BAG3 expression. Methods: BAG3 mRNA and protein were measured using reverse transcription polymerase chain reaction and Western blot in the 2 human gastric cancer cell lines, NUGC3 and MKN28, treated with or without HGF. The effects of BAG3 knockdown on cell proliferation, cell invasion, and apoptosis were analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, the in vitro 2-chamber invasion assay, and flow cytometry in BAG3 short hairpin RNA (shRNA)–transfected cells and control cells. The signaling pathways involved in BAG3 that are regulated by HGF were analyzed. The chromatin immunoprecipitation assay was used to determine binding of Egr1 to the BAG3 promoter. Results: BAG3 mRNA and protein levels were increased following treatment with HGF. HGF-mediated BAG3 upregulation increased cell proliferation and cell invasion; however, it decreased apoptosis. HGF-mediated BAG3 upregulation is regulated by an ERK and Egr1-dependent pathway. BAG3 may have an important role in HGF-mediated cell proliferation and metastasis in gastric cancer through an ERK and Egr1-dependent pathway. Conclusion: This pathway may provide novel therapeutic targets and provide information for further identification of other targets of therapeutic significance in gastric cancer.
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8

An, Ming-Xin, Si Li, Han-Bing Yao, Chao Li, Jia-Mei Wang, Jia Sun, Xin-Yu Li, Xiao-Na Meng, and Hua-Qin Wang. "BAG3 directly stabilizes Hexokinase 2 mRNA and promotes aerobic glycolysis in pancreatic cancer cells." Journal of Cell Biology 216, no. 12 (November 7, 2017): 4091–105. http://dx.doi.org/10.1083/jcb.201701064.

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Aerobic glycolysis, a phenomenon known historically as the Warburg effect, is one of the hallmarks of cancer cells. In this study, we characterized the role of BAG3 in aerobic glycolysis of pancreatic ductal adenocarcinoma (PDAC) and its molecular mechanisms. Our data show that aberrant expression of BAG3 significantly contributes to the reprogramming of glucose metabolism in PDAC cells. Mechanistically, BAG3 increased Hexokinase 2 (HK2) expression, the first key enzyme involved in glycolysis, at the posttranscriptional level. BAG3 interacted with HK2 mRNA, and the degree of BAG3 expression altered recruitment of the RNA-binding proteins Roquin and IMP3 to the HK2 mRNA. BAG3 knockdown destabilized HK2 mRNA via promotion of Roquin recruitment, whereas BAG3 overexpression stabilized HK2 mRNA via promotion of IMP3 recruitment. Collectively, our results show that BAG3 promotes reprogramming of glucose metabolism via interaction with HK2 mRNA in PDAC cells, suggesting that BAG3 may be a potential target in the aerobic glycolysis pathway for developing novel anticancer agents.
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9

McCollum, Andrea K., Giovanna Casagrande, and Elise C. Kohn. "Caught in the middle: the role of Bag3 in disease." Biochemical Journal 425, no. 1 (December 14, 2009): e1-e3. http://dx.doi.org/10.1042/bj20091739.

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Анотація:
Bag3 is a Bag family co-chaperone that regulates the ATPase activity of Hsp70 (heat-shock protein 70) chaperones. Recent studies have demonstrated that Bag3 can initiate macroautophagy in co-operation with small heat-shock protein HspB8. In this issue of the Biochemical Journal, Fuchs and co-workers have discovered the IPV motif in Bag3 that is necessary for binding to HspB8. The authors have also identified HspB6 as a new binding partner for Bag3 and characterized further the binding of both HspB8 and HspB6 in Bag3-mediated clearance of aggregated polyglutamine-containing protein Htt43Q (huntingtin exon 1 fragment with 43 CAG repeats). It is clear from recent identification of a Bag3 mutation that causes a form of muscular dystrophy that the full function of Bag3 in disease is not clear. We will apply the findings of Fuchs et al. in this issue to reconcile the phenotypes of Bag3 homologue knockouts with the emerging role of Bag3 in autophagy.
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10

Lyu, Chuang, Wei-Dong Li, Shu-Wen Wang, Jin-Mei Peng, Yong-Bo Yang, Zhi-Jun Tian, and Xue-Hui Cai. "Host BAG3 Is Degraded by Pseudorabies Virus pUL56 C-Terminal 181L-185L and Plays a Negative Regulation Role during Viral Lytic Infection." International Journal of Molecular Sciences 21, no. 9 (April 29, 2020): 3148. http://dx.doi.org/10.3390/ijms21093148.

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Анотація:
Bcl2-associated athanogene (BAG) 3, which is a chaperone-mediated selective autophagy protein, plays a pivotal role in modulating the life cycle of a wide variety of viruses. Both positive and negative modulations of viruses by BAG3 were reported. However, the effects of BAG3 on pseudorabies virus (PRV) remain unknown. To investigate whether BAG3 could modulate the PRV life cycle during a lytic infection, we first identified PRV protein UL56 (pUL56) as a novel BAG3 interactor by co-immunoprecipitation and co-localization analyses. The overexpression of pUL56 induced a significant degradation of BAG3 at protein level via the lysosome pathway. The C-terminal mutations of 181L/A, 185L/A, or 181L/A-185L/A in pUL56 resulted in a deficiency in pUL56-induced BAG3 degradation. In addition, the pUL56 C-terminal mutants that lost Golgi retention abrogated pUL56-induced BAG3 degradation, which indicates a Golgi retention-dependent manner. Strikingly, BAG3 was not observed to be degraded in either wild-type or UL56-deleted PRV infected cells as compared to mock infected ones, whereas the additional two adjacent BAG3 cleaved products were found in the infected cells in a species-specific manner. Overexpression of BAG3 significantly suppressed PRV proliferation, while knockdown of BAG3 resulted in increased viral yields in HEK293T cells. Thus, these data indicated a negative regulation role of BAG3 during PRV lytic infection. Collectively, our findings revealed a novel molecular mechanism on host protein degradation induced by PRV pUL56. Moreover, we identified BAG3 as a host restricted protein during PRV lytic infection in cells.
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Більше джерел

Дисертації з теми "Ba93"

1

Kingham, Rachel. "The broad-scale impacts of livestock grazing on saltmarsh carbon stocks." Thesis, Bangor University, 2013. https://research.bangor.ac.uk/portal/en/theses/the-broadscale-impacts-of-livestock-grazing-on-saltmarsh-carbon-stocks(a81ba92d-ac40-49c4-ba93-982bffb077d9).html.

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Анотація:
In light of recent upward trends in atmospheric carbon dioxide concentration, efforts have turned to methods of sequestering atmospheric carbon into other stable carbon sinks. Enhancing carbon sequestration by natural systems is an effective way of managing carbon sequestration. Due to high productivity and high sedimentation rates, salt marshes are extremely efficient at capturing and storing carbon, and provide the ideal environment for enhancing carbon sequestration rates through the management of livestock grazing, a common use of salt marshes. However, salt marshes are subject to a range of environmental stressors, which can vary considerably over a large spatial scale . It is therefore important to understand the implications of environmental and contextual variability on the use of livestock grazing as a carbon management tool. Twenty-two salt marshes were selected along the coasts of north Wales and north-west England to assess the impact of grazers on above and below-ground carbon stocks and processes in relation to broader contextual variables. The impacts of seasonality on carbon sequestration rates were also assessed by investigating a salt marsh carbon budget over the course of one year. Grazing was found to have a negative impact on several above-ground plant characteristics, but no impact on soil carbon stocks or overall carbon sequestration rates. Instead, below-ground processes were explained more by the broader environmental variables and seasonal changes. While this study does not discount the fact that grazing may affect soil carbon stocks on the small-scale, or after initial introduction, it shows that grazing impacts are insignificant relative to broader contextual factors on marshes with wellestablished grazing regimes.
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2

De, Marco Margot. "BAG3 role in cardiomyocytes physiopathology." Doctoral thesis, Universita degli studi di Salerno, 2013. http://hdl.handle.net/10556/896.

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Анотація:
2010 - 2011
The anti-apoptotic protein BAG3 is expressed at high levels in skeletal and cardiac muscle in vivo. Our group recently focused its interest on BAG3 role in myocardiocyte proliferation, survival and response to stressful stimuli. We found that BAG3 is upregulated during the differentiation of cardiomyoblasts. Our results prompted us to verify whether bag3 silencing could affect the differentiation state of cardiocytes and we found that bag3 silencing resulted in highly reducing the levels of myogenin. Furthermore, we analyzed BAG3 expression and localization following cell exposure to oxidative stress. In particular, we found that epinephrine in vitro increases BAG3 expression in adult human cardiomyocytes. We evaluated whether BAG3 could be involved in the Tako-tsubo cardiomyopathy (or stress cardiomyopathy) pathogenesis that is characterized by left ventricular dysfunction, with symptoms that can mimic an acute coronary syndrome. The absence of significant cardiovascular risk factors in patients affected by stress cardiomyopathy suggested that it might be associated with a possible genetic etiology. Therefore, we sequenced bag3 gene to check for polymorphisms in 29 patients and 1043 healthy donors. Three polymorphism were highly represented among patients (R71Q, C151R, P407L). We also showed for the first time that BAG3 protein is released from stressed cardiomyocytes and is found in chronic heart failure (HF) patients’ sera. Since anti-BAG3 antibodies are also present in patients’ sera, we developed an ELISA test for their specific detection. In serum samples from chronic HF patients, we found significantly higher values of anti-BAG3 antibodies respect to samples from healthy donors. The presence of anti-BAG3 antibodies in chronic HF patients’ sera and the availability of an ELISA test for their detection can contribute a novel tool for diagnostic and prognostic evaluations. [edited by author]
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3

D'Auria, Raffaella. "BAG3 extracellulare: target cellulari e molecolari." Doctoral thesis, Universita degli studi di Salerno, 2016. http://hdl.handle.net/10556/2355.

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Анотація:
2014 - 2015
Bcl-2-associated athanogene 3 (BAG3) belongs to the family of co-chaperone proteins that interact with the heat shock protein 70 (Hsp70) and is involved in a number of cellular processes including proliferation and apoptosis. BAG3 contains the BAG domain which interacts with the ATPase domain of Hsp70. BAG3 is also characterized by the presence of a WW domain, two conserved Ile-Pro-Val (IPV) motifs and a proline-rich (PXXP) repeat that mediate the binding to partners different from Hsp70. These diverse and multiple interactions underlie the ability of BAG3 to modulate major biological processes such as development, cytoskeleton organization and autophagy. In our laboratory, BAG3 has been recently found in a soluble or membrane-associated form and it has been detected in the serum obtained from patients with pancreatic cancer or heart failure. Moreover, we found that BAG3 is able to bind the cell surface of macrophages and activate the production of inflammatory associated components, such as Nitric Oxide (NO) and Interleukin (IL) -6. To identify novel interacting partners of BAG3 an affinity chromatography on nickel-charged resin was performed, in J774A.1 cells, using recombinant BAG3 (rBAG3) followed by mass spectrometry analysis of the rBAG3-containing complexes. Among these, Interferon- Inducible TransMembrane (IFITM) -2 and Neuropilin (NRP) -1 were the only transmembrane proteins and therefore represented good candidates as receptors for BAG3. Our results show that NRP-1 and IFITM-2 are both essential for the binding of rBAG3 to the cell surface of macrophages and its activation for IL-6 release. We then investigated if BAG3 binding activates some of the signaling pathways known to be involved in macrophage activation. In particular we focused on the phosphatidylinositol 3-kinase (PI3K) and on the p38 pathway that are both involved in Cox-2, iNOS and IL-6 induction in macrophages. We demonstrated that BAG3 signaling is mediated by the receptor complex we identified, since IFITM-2 and/or NRP-1 silencing abrogates BAG3- induced phosphorylation of AKT and p38. We than focus our study on human monocytes, rBAG3 binds the cell surface and induces the release of many pro-inflammatory cytokines and chemokines. Furthermore, we have shown that rBAG3 can bind T lymphocytes cells surface after lipopolysaccharide (LPS) stimulus. All together these findings suggest a role for extracellular BAG3 in immune response. [edited by Author]
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4

Falco, Antonia. "Ruolo della proteina BAG3 nel microambiente tumorale." Doctoral thesis, Universita degli studi di Salerno, 2012. http://hdl.handle.net/10556/293.

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Анотація:
2009 - 2010
Recenti studi hanno dimostrato che il microambiente tumorale subisce numerosi cambiamenti nel corso dello sviluppo del tumore e influenza l’evoluzione e la progressione del cancro. L'ambiente ipossico del tumore stimola l'angiogenesi che può direttamente promuovere la sopravvivenza delle cellule tumorali e la loro invasione. Anche l'infiltrato infiammatorio, associato a molti tumori solidi, è in grado di modulare il comportamento delle cellule tumorali, con effetti anti- e pro-tumorali. Un ruolo importante è svolto anche dai fibroblasti che circondano il tumore, i quali sono in grado di rilasciare fattori di crescita e citochine che stimolano l’ angiogenesi, la crescita del tumore e l'invasione. Tutti questi componenti sono potenziali bersagli per nuove strategie terapeutiche, e, infatti, diverse molecole che agiscono su tali target, sono attualmente utilizzate nelle sperimentazioni cliniche. Inoltre, dati recenti dimostrano che alcuni componenti del microambiente tumorale sono in grado di fornire importanti informazioni prognostiche e predittive. A tale scopo diventa sempre più evidente che, una caratterizzazione completa delle molecole e delle cellule coinvolte nel microambiente del tumore, è richiesta per una maggiore conoscenza della biologia del tumore. BAG3 è una proteina citoplasmatica che è stata recentemente caratterizzata per il suo ruolo centrale in diversi processi associati al tumore quali la sopravvivenza, la proliferazione, la migrazione e l'autofagia. Il ruolo di BAG3 nel microambiente associato al tumore non è stato caratterizzato finora. Pur non avendo un dominio transmembrana, i nostri studi hanno dimostrato che BAG3 può essere associata alla membrana plasmatica e rilasciata nel mezzo extracellulare di alcune cellule neoplastiche e in particolare cellule tumorali del pancreas. Abbiamo anche confermato la presenza di una forma extracellulare di BAG3 nel siero di pazienti affetti da adenocarcinoma pancreatico. Dopo il rilascio nello spazio extracellulare, BAG3 può legare la superficie di cellule adiacenti al tumore, e in particolare abbiamo cercato di stabilire se BAG3 può avere un effetto sui macrofagi che svolgono un ruolo importante nel microambiente infiammatoria associato al tumore. Abbiamo trovato che BAG3 è in grado di legare la superficie cellulare dei macrofagi e di indurre la produzione di componenti associati al processo infiammatorio. Abbiamo anche individuato un nuovo ruolo per BAG3 intracellulare nella regolazione della neo-angiogenesi. Infatti, abbiamo dimostrato che BAG3 è espressa nelle cellule endoteliali e che è in grado di regolare la proliferazione cellulare interagendo con ERK1/2 e la sua fosfatasi DUSP6. Come conseguenza, la riduzione di BAG3 determina una sostenuta fosforilazione di ERK1/2 e una ridotta crescita delle cellule endoteliali in vitro e in vivo. Questo, a sua volta induce una ridotta crescita del tumore in vivo in conseguenza alla ridotta angiogenesi. Complessivamente questi risultati permettono di individuare per la proteina BAG3 un ruolo nuovo nella regolazione dello sviluppo del tumore. [a cura dell'autore]
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5

Myers, Valerie. "The Role of BAG3 in the Failing Heart." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/490584.

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Анотація:
Biomedical Sciences
Ph.D.
Heart disease has been the leading cause of death in the United States for more than 90 years. The leading cause of death in individuals aged 65 and older has remained diseases of the heart from 1950 to the current time. According to the CDC, once diagnosed with heart disease, individuals have an approximately 50% chance of dying within 5 years, regardless of race. Mortality related to heart disease increased dramatically from the start of the 1900s to 1921, but subsequently experienced a steady decline from the mid-1960’s to 2000. However, when the decrease in heart disease is examined at the level of race it is clear that the decrease is not equally shared. While the leading cause of death among both Caucasian American men and women and African American men and women remains heart disease, the decrease in incidence of coronary heart disease among African American men was only half of the decrease in incidence among Caucasian American men. Genetic variants in BAG3 (Bcl-2 associated athanogene 3), a highly evolutionarily conserved gene that has recently emerged as a major dilated cardiomyopathy locus, are prevalent in isolated populations. This led us to hypothesize that variants in BAG3 might contribute to the increased prevalence of IDC in individuals of African ancestry. Expressed predominantly in the heart, the skeletal muscle and in many cancers, BAG3 has pleotropic effects in the heart. It inhibits apoptosis by binding to Bcl-2, facilitates protein quality control by binding to both large and small heat shock proteins, mediates adrenergic responsiveness by coupling the β-adrenergic receptor and the L-type Ca2+ channel, and maintains the integrity of the sarcomere by anchoring actin filaments to the Z disc. However, a paucity of subjects of African ancestry have been included in cohorts of probands with familial dilated cardiomyopathy whose exomes or genomes have been sequenced. Based on our previous observations and reports from other groups we postulated: 1) that mice with haplo-insufficiency of BAG3 will re-capitulate disease seen in humans and serve as a model for studying the pathogenesis of BAG3. 2) The prevalence or identification of specific BAG3 variants will differ by race and/or ethnicity. 3) SNVs of BAG3 may contribute to disease progression and thereby be pathogenic. Our study points out that we cannot understand population-based differences without enhancing the diversity of populations included in genomic studies. Similarly, in the era of big data, efforts must be undertaken to assess the genetic profile of both probands and their family members as without the ability to measure segregation, penetrance and plasticity we can only ascribe associations to functional genetic variants.
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6

Engelmann, Ines. "Änderung der Stoffwechselaktivität von BaF3-Zellen durch die Expression von BCR/ABL." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-163535.

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Die vorliegende Arbeit handelt von einer in vitro Untersuchung der Stoffwechselveränderun-gen durch die Expression von BCR/ABL bei BaF3-Zellen, einer murinen, IL-3-abhängigen B-Zelllinie. Die Zellen wurden in nährstoffreichem Standard- und in durch Titrationen ermittel-tem nährstoffarmem Minimalmedium auf unterschiedliche Stoffwechselaktivität in Abhän-gigkeit von BCR/ABL-Expression untersucht sowie auf die zusätzliche Beeinflussbarkeit durch IL-3. Danach wurden vergleichend zwischen den 2 Zelllinien (BaF3 und BaF3-BCR/ABL) im Minimalmedium und im Standardmedium Metabolite wie Glukose, Laktat und Aminosäuren bestimmt, wobei BaF3-BCR/ABL sowohl mit als auch ohne IL-3 kultiviert wur-de. Um den Einfluss von Nährstoffrestriktion auf die Therapie zu zeigen, wurden anschlie-ßend vergleichend in den beiden Medien die Tyrosinkinaseinhibitoren Imatinib und Nilotinib titriert. Die Ergebnisse zeigen, dass BaF3-BCR/ABL einen Wachstumsvorteil im Minimalmedium hat, welcher im Standardmedium nicht vorliegt. Während die bereits bekannte Verstärkung der Glukoseaufnahme durch BCR/ABL im Standardmedium bestätigt wurde, konnte im Minimal-medium Gegenteiliges gezeigt werden. Zudem wurde ein Unterschied im Aminosäurestoff-wechsel zwischen BaF3 + IL-3 und BaF3-BCR/ABL + IL-3 im Minimalmedium deutlich. Die therapeutische Relevanz des gezeigten Einflusses der Nährstoffrestriktion konnte anschlie-ßend in der Tyrosinkinaseinhibitortitration dargestellt werden, da die Medikamente in Abhän-gigkeit vom Medium unterschiedliche Wirkungen zeigen. Insgesamt bieten die Ergebnisse einen metabolischen Erklärungsansatz für das Überleben von Tumorstammzellen in nährstoffarmen Arealen des Knochenmarks unter Therapie und Raum für neue Therapieansätze.
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Korniat, Agathe. "Etude fonctionnelle des variants moléculaires du gène BAG3 associés à la cardiomyopathie dilatée humaine." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066716.

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Le gène BAG3 a été identifié comme étant un nouveau gène responsable de cardiomyopathie dilatée (CMD), première cause d'insuffisance cardiaque (IC). La protéine BAG3 est une co-chaperonne qui participe au contrôle de l'homéostasie protéique via son rôle dans l'autophagie, protégeant ainsi les cellules contre la protéotoxicité induite par les protéines dégradées ou mal repliées. L'hypothèse qu'une inactivation de la voie autophagique contrôlée par BAG3 induirait une protéotoxicité cardiomyocytaire à l'origine de la CMD apparait particulièrement attractive et constitue l'hypothèse centrale de ce travail. Nos résultats indiquent que les mutations de BAG3 abolissent l'interaction avec la chaperonne HSP70, une protéine centrale du contrôle qualité des protéines. Nous avons observé une cytotoxicité des mutants BAG3, une altération de la fonction chaperonne HSP70-dépendante et une absence de réponse autophagique en condition de stress (jeun, choc thermique, expression d'une protéine pro-agrégante). In vivo (modèle poisson-zèbre) l'extinction de l'expression de BAG3 ou la surexpression des mutants conduisent à l'apparition d'un phénotype d'insuffisance cardiaque (¿dème péricardique) chez les embryons injectés. Par édition génomique, nous développons également un modèle de cardiomyocytes dérivés de cellules iPS porteurs ou non de la mutation afin d'explorer plus en avant la fonction contractile de ces cellules. Nos résultats confirment donc le rôle de BAG3 dans la CMD et indiquent que l'altération de la fonction protéostasique serait à l'origine de la maladie. Cette nouvelle voie physiopathologique dans la CMD pourrait s'avérer être, plus généralement, une voie centrale dans l'IC
The BAG3 gene was identified as a novel gene responsible for dilated cardiomyopathy (DCM), a major cause of heart failure (HF). The BAG3 protein is a co-chaperone that participates in the control of protein homeostasis via its role in autophagy, protecting cells against the proteotoxicity induced by degraded or misfolded proteins. The hypothesis that inactivation of the autophagic pathway controlled by BAG3 would induce cardiomyocyte proteotoxicity behind the CMD appears particularly attractive and is the central hypothesis of this work. Our results indicate that BAG3 mutations abolish the interaction with the chaperone HSP70, a central actor of the protein quality control. We observed cytotoxicity of BAG3 mutants, an impaired HSP70-dependent chaperone function and absence of autophagic response under stress conditions (starvation, heat shock, expression of a pro-aggregating protein). In vivo (zebrafish model) the extinction of BAG3 expression or mutants overexpression lead to the occurrence of a heart failure phenotype (pericardial edema) in injected embryos. Through genomic edition, we also develop a model of iPS-derived cardiomyocytes carrying or not the mutation in order to further explore the contractile function of these cells. Our results confirm the role of BAG3 in DCM and indicate that the alteration of the proteostasis function is the cause of the disease. This new pathophysiological pathway in DCM may prove to be more generally, a central line in the IC
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Manchen, Steven T. "Characterization and subcellular localization of the human BAT3 protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62248.pdf.

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9

Isaksen, Katja. "Consumer culture, branding and British adolescents : a vicious cycle? : a comparison between high and low-income adolescents." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/consumer-culture-branding-and-british-adolescents-a-vicious-cycle-a-comparison-between-high-and-lowincome-adolescents(94a6b8e2-c339-447b-ba93-110b4dc22755).html.

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The growth of consumerism has meant that individuals are increasingly using possessions as a means of developing their personal identities and forming social connections. Specifically, the consumer culture has seen the increase of brands and branded goods as marketers attach emotional attributes to them. Thus, brands have become communicative symbols which display, amongst other things, the owner's values, beliefs and social status. As a result, consumers are attempting to form their identities, social connections and self-worth by consuming (often branded) possessions which they feel are representative of their self or ideal self and will increase their chances of social acceptance. However, psychological studies in consumer behaviour suggest that the increasing propensity to seek inner happiness and social bonds through external means (consumption), has led consumers to be less satisfied with their lives and hence decreases psychological well-being; the focus on external rewards has reduced the importance that individuals place on personal development and intrapsychic developments.This study investigates the relationship between the consumption culture, branding and British adolescents, with a comparison between high and low-income teenagers. Adolescents are particularly prone to assuming consumer orientations (and hence the consequences thereof) due to their stage in identity development, their need for social acceptance and the fact that they are a very profitable market segment. As a result, teenagers are encouraged to turn to consumption for developing their personal and social identities, as opposed to more traditional means such as personal skill development. Although limited studies have investigated adolescent consumption, little attention has been paid to low-income adolescents who are prone to reduced self-worth but have a restricted consumption scope and thus cannot consume their self-worth in the same 'normal' ways as their peers. In light of previous studies, it was necessary to first develop a new measure of self-esteem which included the vital role of possessions (and specifically brands) in feelings of self-worth amongst adolescents. The scale-development process revealed the functional importance of self-esteem as a marker of social inclusion and hence shed light on the reason for the importance that adolescents place on specific brands; they are a promise of fitting-in. A valid and reliable 23-item, self-report measure of self-esteem is presented. Subsequent to developing the new scale, the research provided empirical support for a model of the psychological characteristics of adolescent consumption (including self-esteem). The result is a 'Vicious Cycle' model of consumption which suggests that there is a relationship between the factors which contribute to a consumer orientation and the likely effects of having such an orientation. For example, the model suggests that reduced self-esteem may contribute to consumerism and a consumption orientation may contribute to a reduction in self-esteem. Furthermore, the comparison between high and low-income teenagers showed that low-income teenagers were significantly more materialistic than their high-income counterparts thus supporting the suggestion that low-income teenagers are more prone to consumerism than their high-income counterparts. With reference to the detailed links presented in the Vicious Cycle model, the author proceeds to explore the efficacy of extant consumerist-curbing strategies and highlight the need for more effective methods if we wish future generations to develop in to more than simply shoppers.
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Peña, Oyarzún Daniel. "Rol de BAG3 en la regulación del metabolismo muscular esquelético." Tesis, Universidad de Chile, 2014. http://repositorio.uchile.cl/handle/2250/134613.

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Memoria para optar el título de Bioquímico
Autor no autoriza el acceso a texto completo de su documento hasta diciembre de 2015
La proteína co-chaperona Bag3 es un factor clave en el control de la autofagia selectiva, un proceso de degradación de proteínas y organelos activado en respuesta a distintos estresores, en tejidos altamente diferenciados, como el músculo esquelético. Este último tejido transforma la energía química del ATP en energía mecánica para la contracción, por lo que el control del metabolismo de la glucosa resulta fundamental para mantener su función fisiológica. En este sentido, insulina, a través de sus efectores intracelulares Akt y mTORC1, promueve el ingreso y metabolismo de la glucosa. No obstante, en condiciones de estrés nutricional la proteína AMPK activa la autofagia para aumentar el metabolismo celular por degradación de diversas macromoléculas. Prueba de esta relación funcional entre metabolismo y autofagia es que la inhibición de la autofagia lleva a resistencia a la insulina en células musculares esqueléticas. Por otro lado, existe evidencia que los ratones knock-out para Bag3 presentan una disminución en los niveles de glucosa e insulina circulantes, y mueren a las 3 semanas de nacimiento con deterioro muscular progresivo. Sin embargo, hasta hoy se desconoce si Bag3 regula el metabolismo energético de la célula, y si las vías que controlan ese metabolismo se relacionan con la autofagia. En vista de estos antecedentes, se investigó si Bag3 altera la señalización de la vía Akt-AMPK-mTORC1, produciendo efectos metabólicos y de autofagia en miotubos L6 (línea celular: músculo esquelético de rata). A través de ensayos de captura de 3H-2-desoxiglucosa, consumo de oxígeno y detección densitométrica de GLUT4-myc en superficie, se determinó que las células con niveles reducidos de Bag3 (RNA interferente) y sin insulina en el sistema, incorporaron mayor cantidad de glucosa por un incremento de transportadores Glut-4 en la membrana celular junto con una mayor capacidad oxidativa mitocondrial. Lo anterior es debido a un aumento de la activación basal de Akt, evidenciado por Western blot contra Fosfo-Ser-473. Además, estas células presentaron una menor capacidad de activar la autofagia debido a un procesamiento disminuido de LC3, además de una menor activación de AMPK (Fosfo-Thr-172) y una sobre-activación de mTORC1 (Fosfo-Ser-2448). Finalmente, en presencia de insulina (100 nM, 20 min), las células con niveles reducidos de Bag3 presentaron una incorporación deficiente de glucosa para la cantidad de transportador Glut-4 exportado a la membrana, y una menor capacidad oxidativa mitocondrial. En estas condiciones, Akt se activó de forma normal ante insulina, observándose sin embargo que AMPK y mTORC1 se activó e inactivó, respectivamente; comportamiento inverso respecto a lo normal. Con estos datos, se propone a Bag3 como un novedoso regulador del metabolismo y la autofagia muscular esquelética
The co-chaperone protein Bag3 is a key factor for the control of selective autophagy, a degradation process of proteins and organelles activated in response to stress, in highly differentiated tissues, as the skeletal muscle. The role of the latter is to transform the chemical energy from ATP into mechanical energy for contraction, thus the metabolism control of glucose is important to keep its biological function. In that way, the hormone insulin, by its intracellular effectors Akt and mTORC1, promotes the uptake and metabolism of glucose. However, in nutritional stress conditions the AMPK protein activate autophagy in order to increase cellular metabolism by macromolecular degradation. Proof of this functional relationship between metabolism and autophagy is that autophagy abrogation leads to insulin resistance in muscle cells. On the other hand, there is evidence that shows that Bag3 Knock-out mice present diminished glucose and insulin in blood, and die after 3 weeks from birth with progressive muscle wasting. However, it is not known yet whether Bag3 regulates energy metabolism in the cell, nor whether the pathways that control that metabolism are related with Bag3 mediated autophagy. With this in mind, we decided to determine if Bag3 was able to alter the Akt-AMPK-mTORC1 signaling pathway, leading to metabolic and autophagy effects, in L6 myotubes (cell line: skeletal muscle from rat). By 3H-2-desoxyglucose uptake, oxygen consumption and GLUT4-myc surface detection assays, we were able to determine that cells with reduced levels of Bag3 (interference RNA), and without insulin in the system, had increased glucose uptake because of an augmented Glut-4 translocation to the cell membrane, along with an enhanced mitochondrial oxidative capacity. This is explained by an increased Akt basal activation, evidenced by Phospho-Ser-473 western blot. Furthermore, these cells showed a diminished capacity to produce autophagy, because of a decreased LC3 processing, along with a diminished activation of AMPK (Phospho-Thr-172) and an over activation of mTORC1 (Phospho-Ser-2448). Finally, in the presence of insulin (100 nM, 20 minutes), cells with diminished levels of Bag3 showed a deficient glucose uptake for the amount of Glut-4 transporter exported to cell membrane, and a decreased mitochondrial oxidative capacity. Under these conditions, Akt protein increased its activation, as normal, but AMPK was activated and mTORC1 was inactivated, an inverted behavior with respect to normal metabolism. With these data, we propose Bag3 as a novel regulator of metabolism and autophagy in muscle
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Книги з теми "Ba93"

1

Ratā, Dāwit Neguśu. Ba97 ʼenā léločem. ʼAdis ʼAbabā: Dértogādā mātamiyā bét, 2014.

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Jossey-Bass Handbook of Nonprofit Leadership and Management. Wiley & Sons, Incorporated, John, 2016.

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Jossey-Bass Handbook of Nonprofit Leadership and Management. Wiley & Sons, Incorporated, John, 2024.

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The Jossey-Bass Handbook of Nonprofit Leadership and Management. 3rd ed. San Francisco: Jossey-Bass, 2010.

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Starting and Managing a Nonprofit Organization: A Legal Guide. Wiley & Sons, Incorporated, John, 2017.

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Dasgupta, Probal, Jesper Lykke Jacobsen, and István Ertl. Beletra Almanako 43 (BA43 - Literaturo en Esperanto). Mondial, 2022.

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7

Mitoseriu, Liliana, and Adelina Ianculescu. BaO3 - Functional Materials: From Nanopowders to Bulk Ceramics. Nova Science Publishers, Incorporated, 2010.

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Media, BPP Learning. CIMA BA3 Fundamentals of Financial Accounting: Passcards. BPP Learning Media, 2020.

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Media, BPP Learning. CIMA BA3 Fundamentals of Financial Accounting: Passcards. BPP Learning Media, 2019.

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Media, BPP Learning. CIMA BA3 Fundamentals of Financial Accounting: Passcards. BPP Learning Media, 2021.

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Частини книг з теми "Ba93"

1

Villars, P., K. Cenzual, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk, and R. Zaremba. "Ba3[In2F12] α." In Landolt-Börnstein - Group III Condensed Matter, 501. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22847-6_419.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "Ba3[PO4]2." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 647–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_524.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "Ba3(V0.5W0.5)2O8.5." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 669. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_543.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, and I. Savysyuk. "Ba3(B3O6)2 rt." In Structure Types. Part 9: Space Groups (148) R-3 - (141) I41/amd, 405. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02702-4_288.

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Villars, P., K. Cenzual, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk, and R. Zaremba. "Ba3[Co(H2O)BW11O39]∙26H2O." In Landolt-Börnstein - Group III Condensed Matter, 430. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22847-6_352.

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Villars, P., K. Cenzual, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk, and R. Zaremba. "Ba3[Ti(O2)F5]2∙2H2O." In Landolt-Börnstein - Group III Condensed Matter, 60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22847-6_15.

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7

Behl, Christian. "The role of the co-chaperone BAG3 in selective macroautophagy: implications for aging and disease." In Protein Quality Control in Neurodegenerative Diseases, 87–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27928-7_7.

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8

Pascale, Maria, Alessandra Rosati, Michelina Festa, Anna Basile, Morena d’Avenia, Antonia Falco, Gaetano Torino, and Maria Caterina Turco. "BAG3 Protein: Role in Some Neoplastic Cell Types and Identification as a Candidate Target for Therapy." In Apoptosome, 137–46. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3415-1_7.

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Pinakoulaki, Eftychia, Ute Pfitzner, Thomas Osterman, Bernd Ludwig, and Costas Varotsis. "Resonance Raman scattering from cytochromes aa3 and ba3 in the fully oxidized cytochrome oxidase /H2O2 reaction." In Spectroscopy of Biological Molecules: New Directions, 195–96. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4479-7_86.

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Pinakoulaki, Eftychia, Thomas Ostermann, Bernd Ludwig, and Costas Varotsis. "Cytochrome a3 hemepocket relaxation subsequent to carbon monoxide photolysis from fully reduced cytochrome ba3 oxidase of Paracoccus denitrificans." In Spectroscopy of Biological Molecules: New Directions, 197–98. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4479-7_87.

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Тези доповідей конференцій з теми "Ba93"

1

Xu, Jun. "Raman and optical spectra of Mn5+-doped Ba3 (Vo4) 2 and Ba3 (v1xTaxo4)." In 17th Congress of the International Commission for Optics: Optics for Science and New Technology. SPIE, 1996. http://dx.doi.org/10.1117/12.2316003.

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Racu, Andrei, Marius Stef, Irina Nicoara, Daniel Vizman, and Gabriel Buse. "Photoluminescence and Judd-Ofelt analysis of ErF3–doped BaF3 crystals." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.15.4.

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Rosati, Alessandra, Anna Basile, Raffaella D'Auria, Morena d'Avenia, Margot De Marco, Antonia Falco, Michelina Festa, et al. "Abstract 2393: PDAC cells release BAG3 that activates a paracrine loop with stromal macrophages." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2393.

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Clarke, Stanley R., Allie H. Naccara, Amanda J. Loya, Sam W. Marchant, Xiaoou Wang, Thomas J. LaJoie, Jordyn N. Smith, and Kevin P. Rice. "Abstract 266: Relationship between BAG3 expression and the cytotoxicity of laromustine in HL60 cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-266.

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Clarke, Stanley R., Allie H. Naccara, Amanda J. Loya, Sam W. Marchant, Xiaoou Wang, Thomas J. LaJoie, Jordyn N. Smith, and Kevin P. Rice. "Abstract 266: Relationship between BAG3 expression and the cytotoxicity of laromustine in HL60 cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-266.

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6

Bareduan, S. A., and S. H. Hasan. "Bottleneck adjacent matching 3 (BAM3) heuristic for re-entrant flow shop with dominant machine." In 2008 IEEE International Conference on Industrial Engineering and Engineering Management (IEEM). IEEE, 2008. http://dx.doi.org/10.1109/ieem.2008.4737848.

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Li, Zeqian. "Silencing BAG3 Inhibits Tumor Cell Proliferation by reducing the Activation of ERK in TNBC." In ISAIMS 2022: 2022 3rd International Symposium on Artificial Intelligence for Medicine Sciences. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3570773.3570886.

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Feced, R., M. K. Durkin, M. Ibsen, and M. N. Zervas. "An efficient inverse scattering algorithm for the synthesis of the response of fibre-gratings." In Bragg Gratings, Photosensitivity, and Poling in Glass Waveguides. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/bgpp.1999.ba3.

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De Laurenzi, Vincenzo, Alessandra Rosati, Gianluca Sala, and Maria Caterina Turco. "Abstract LB-A14: Targeting BAG3-dependent paracrine loop reduces growth and metastatic spreading of Pancreatic adenocarcinoma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-lb-a14.

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Schumann, E., L. Gulatz, D. Zengeler, S. Gräf, S. Rupp, and A. Schänzer. "Gestörte kardiale Autophagie bei einer kardio-skeletalen Myofibrillären Myopathie im Kindesalter aufgrund einer BAG3 (Pro209Leu) Mutation." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685097.

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