Gotowa bibliografia na temat „Netrin-1 (NTN1)”
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Artykuły w czasopismach na temat "Netrin-1 (NTN1)"
Schlegel, Martin, Monika Sharma, Emily J. Brown, Alexandra A. C. Newman, Yannick Cyr, Milessa Silva Afonso, Emma M. Corr i in. "Silencing Myeloid Netrin-1 Induces Inflammation Resolution and Plaque Regression". Circulation Research 129, nr 5 (20.08.2021): 530–46. http://dx.doi.org/10.1161/circresaha.121.319313.
Pełny tekst źródłaDudgeon, Crissy, Anthony Casabianca, Chris Harris, Igor Astsaturov, Charline Ogier, Xiaoyang Su, Jason Pitarresi i in. "Abstract B020: Retinoic acid produced by hepatic stellate cells facilitates Netrin-1 mediated pancreatic cancer metastasis". Cancer Research 82, nr 22_Supplement (15.11.2022): B020. http://dx.doi.org/10.1158/1538-7445.panca22-b020.
Pełny tekst źródłaOchiai, Yosuke, Sunagawa Masaki, Ermanno Malagola, Hiroki Kobayashi, Feijing Wu, Ruth A. White, Leah B. Zamechek i Timothy C. Wang. "Abstract B100: Netrin-1/Neogenin-1 interaction modulates pancreatic innervation to promote tumorigenesis and accelerates cancer progression". Cancer Research 84, nr 2_Supplement (16.01.2024): B100. http://dx.doi.org/10.1158/1538-7445.panca2023-b100.
Pełny tekst źródłaWang, Ligang, Lingling Zhao, Longchao Zhang, Xin Liu, Xinhua Hou, Hongmei Gao, Hua Yan, Fuping Zhao i Lixian Wang. "NTN1 Affects Porcine Intramuscular Fat Content by Affecting the Expression of Myogenic Regulatory Factors". Animals 9, nr 9 (27.08.2019): 609. http://dx.doi.org/10.3390/ani9090609.
Pełny tekst źródłaGarcia Galindo, Jesús Jonathan, Maria G. Ramos-Zavala, Sara Pascoe-Gonzalez, Sandra O. Hernández-González, J. Santiago Delgadillo-Centeno, Fernando Grover-Páez, Alberto Beltrán-Ramírez i Daniel O. Suarez Rico. "Association of Netrin 1 with hsCRP in Subjects with Obesity and Recent Diagnosis of Type 2 Diabetes". Current Issues in Molecular Biology 45, nr 1 (26.12.2022): 134–40. http://dx.doi.org/10.3390/cimb45010010.
Pełny tekst źródłaLi, Dandan, Guirong Zhu, Shu Lou, Lan Ma, Chi Zhang, Yongchu Pan i Lin Wang. "The functional variant of NTN1 contributes to the risk of nonsyndromic cleft lip with or without cleft palate". European Journal of Human Genetics 28, nr 4 (28.11.2019): 453–60. http://dx.doi.org/10.1038/s41431-019-0549-4.
Pełny tekst źródłaMirakaj, Valbona, Jesmond Dalli, Tiago Granja, Peter Rosenberger i Charles N. Serhan. "Vagus nerve controls resolution and pro-resolving mediators of inflammation". Journal of Experimental Medicine 211, nr 6 (26.05.2014): 1037–48. http://dx.doi.org/10.1084/jem.20132103.
Pełny tekst źródłaMentxaka, Amaia, Javier Gómez-Ambrosi, Beatriz Ramírez, Amaia Rodríguez, Sara Becerril, Gabriela Neira, Víctor Valentí i in. "Netrin-1 Promotes Visceral Adipose Tissue Inflammation in Obesity and Is Associated with Insulin Resistance". Nutrients 14, nr 20 (18.10.2022): 4372. http://dx.doi.org/10.3390/nu14204372.
Pełny tekst źródłaMentxaka, Amaia, Javier Gómez-Ambrosi, Gabriela Neira, Beatriz Ramírez, Sara Becerril, Amaia Rodríguez, Víctor Valentí i in. "Increased Expression Levels of Netrin-1 in Visceral Adipose Tissue during Obesity Favour Colon Cancer Cell Migration". Cancers 15, nr 4 (7.02.2023): 1038. http://dx.doi.org/10.3390/cancers15041038.
Pełny tekst źródłaShiovitz, Stacey, Li Hsu, Conghui Qu, Tabitha A. Harrison, Sonja Berndt, Hermann Brenner, Graham Casey i in. "DCC and RET pathway analysis to identify factors associated with advanced colorectal cancer." Journal of Clinical Oncology 32, nr 3_suppl (20.01.2014): 457. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.457.
Pełny tekst źródłaRozprawy doktorskie na temat "Netrin-1 (NTN1)"
Chicherova, Ievgeniia. "Netrin-1 and neurons in hepatocellular carcinoma". Electronic Thesis or Diss., Lyon, 2022. https://n2t.net/ark:/47881/m60r9pbg.
Pełny tekst źródłaChronic liver inflammation can lead to chronic liver diseases (CLD), including hepatitis, cirrhosis and hepatocellular carcinoma (HCC), which is the most common malignant primary liver tumor and is the 3rd most common cancer in terms of mortality worldwide. Regardless of the etiological factor all CLDs share numerous common patho-physiogycal mechanisms: unfolded protein response (UPR), chronic inflammation and fibrosis. Using animal model and clinical samples we studied another common denominator of CLDs and HCC, which is the system of axon guidance cue netrin-1 and its dependence receptors UNC5s. Netrin-1, known as pro-oncogenic in other solid tumors, is induced during hepatic inflammation, and the pro-apoptotic signal of UNC5 receptors is attenuated with overall increased ligand/receptor balance in cirrhosis and HCC. Chronic inflammation is mediated by multiple actors of the immune system. The implication of autonomic nervous system (ANS) in hepatic inflammation and CLD progression remains poorly understood. Looking at the involvement of pre-synaptic and post-synaptic neuronal signals in the cirrhosis and HCC, we observed the reshaping of the balance between intrahepatic sympathetic (adrenergic) and parasympathetic (cholinergic) nervous systems. In vivo model of cirrhotic HCC showed the progressive establishment of cholinergic orientation throughout the different stages of fibrosis. The overall cholinergic signal of HCC was associated with anti-inflammatory microenvironment and poorer survival in patients. The observed CLD-to-HCC progression in vivo was accompanied by the overexpression of immature neuronal markers in HCC. Altogether, we showed that the parasympathetic arm of the ANS is implicated in the patho-physiology of HCC, and encourage for the use of ANS-targeting drugs in HCC studies, many of which are clinically safe and well characterized. Trying to establish the connection between pro-survival and chemotactic netrin-1 and intrahepatic ANS, we found the positive association between netrin-1/UNC5s and cholinergic signal in HCC. Netrin-1 targeting by the monoclonal antibody NP137, currently studied in the clinical trials in the treatment of advanced solid tumors, showed remodeling of ANS orientation, confirming the sensitivity of ANS to netrin-1/UNC5 axis in the hepatic pathological context. The most common molecular anomalies in HCC in the TERT promoter and CTNNB1 gene, showed an association with netrin-1/UNC5 system, whereas mutations in T53, the well-known regulator of NTN1 and UNC5s expression did not show any implication in netrin-1/UNC5 axis reshuffling in clinical HCC samples, also unsensitive to functionality status of p53. In average, CTNNB1-mutated clinical samples correlated with adrenergic polarity of HCC, whereas TP53 mutations appear to be positively associated with cholinergic polarity of HCC. Taken together, my thesis results suggest the putative pro-cancerogenic role of the netrin-1 and the implication of the neuroregulation via ANS in the CLD and HCC development