image3_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

presentation1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.pptx by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

presentation1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.pptx by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image3_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image1_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image3_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image2_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

image2_Myostatin Promotes Osteoclastogenesis by Regulating Ccdc50 Gene Expression and RANKL-Induced NF-κB and MAPK Pathways.tif by Xin Zhi (1829224)

“…Specifically, myostatin increased the phosphorylation of Smad2, which led to the activation of NF-κB and MAPK pathways to activate osteoclastogenesis. Ccdc50 was identified as a gene whose expression was highly decreased in osteoclastogenesis upon myostatin treatment, and it could inhibit the function of myostatin in osteoclastogenesis by blocking NF-κB and MAPKs pathways. …”

Salience of authority-virtue phrases by year. by Daniel Hart (440152)

Decreased neutrophil and monocyte antigen expression in the paws of anti-S100A9-treated mice. by Annabelle Cesaro (112070)

Baseline level biochemical and circulating biomarkers in study subjects. by Jaskiran Kaur (160829)

Change in serum levels of vitamin D and angiogenic marker at 16 weeks follow-up. by Jaskiran Kaur (160829)

Blood pressures (mmHg) in isopropyl alcohol exposed workers and controls. by Zhiqiang Zhao (201543)

Inverse Relationship between IGF-1 induced Cyr61 upregulation and decreased E-cadherin and FOXO1 expression is confirmed in two cell lines. by Suren Sarkissyan (388555)

Expression levels of M2 macrophage markers regulated by PI3K-AKT signaling pathway are significantly decreased by Tipe2-deficient macrophages. by Ruiling Liu (507091)

DataSheet5_First-Line ICI Monotherapies for Advanced Non-small-cell Lung Cancer Patients With PD-L1 of at Least 50%: A Cost-Effectiveness Analysis.docx by Qiao Liu (346535)

“…</p><p>Conclusion: For advanced NSCLC patients with PD-L1 of at least 50%, cemiplimab was a cost-effective option compared with pembrolizumab and a dominant alternative against atezolizumab. …”

DataSheet2_First-Line ICI Monotherapies for Advanced Non-small-cell Lung Cancer Patients With PD-L1 of at Least 50%: A Cost-Effectiveness Analysis.docx by Qiao Liu (346535)

“…</p><p>Conclusion: For advanced NSCLC patients with PD-L1 of at least 50%, cemiplimab was a cost-effective option compared with pembrolizumab and a dominant alternative against atezolizumab. …”

DataSheet3_First-Line ICI Monotherapies for Advanced Non-small-cell Lung Cancer Patients With PD-L1 of at Least 50%: A Cost-Effectiveness Analysis.docx by Qiao Liu (346535)

“…</p><p>Conclusion: For advanced NSCLC patients with PD-L1 of at least 50%, cemiplimab was a cost-effective option compared with pembrolizumab and a dominant alternative against atezolizumab. …”