Lu Zhang

ORCID: 0009-0004-4606-4277
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About
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Research Areas
  • Chronic Myeloid Leukemia Treatments
  • RNA Research and Splicing
  • MicroRNA in disease regulation
  • Neuroblastoma Research and Treatments
  • Cell death mechanisms and regulation
  • Cardiac Ischemia and Reperfusion
  • Inflammatory Biomarkers in Disease Prognosis
  • Anesthesia and Neurotoxicity Research
  • Cardiovascular and exercise physiology
  • Cardiac Health and Mental Health
  • Cancer Risks and Factors
  • Hepatitis Viruses Studies and Epidemiology
  • Virus-based gene therapy research
  • Head and Neck Cancer Studies
  • Herpesvirus Infections and Treatments
  • Cancer therapeutics and mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms

Qilu Hospital of Shandong University
2010-2024

Shandong University
2014

Background Obesity abolishes anesthetic pre‐conditioning‐induced cardioprotection due to impaired reactive oxygen species ( ROS )‐mediated adenosine monophosphate‐activated protein kinase AMPK ) pathway, a consequence of increased basal myocardial oxidative stress. Exercise training has been shown attenuate obesity‐related Objective This study tests whether exercise could normalize ‐mediated pathway and prevent the attenuation in obesity. Methods Male S prague– D awley rats were divided into...

10.1111/aas.12414 article EN Acta Anaesthesiologica Scandinavica 2014-10-14

Neuroblastoma is a solid tumor that occurs mainly in children. Malignant neuroblastomas have poor prognosis because conventional chemotherapeutic agents are not very effective. Survivin, member of the inhibitor apoptosis protein family, plays significant role cell division, inhibition apoptosis, and promotion proliferation invasion. Previous studies found survivin highly expressed some malignant correlated with prognosis. The aim this study was to investigate whether could serve as potential...

10.1590/1414-431x20143459 article EN cc-by Brazilian Journal of Medical and Biological Research 2014-05-22

Abstract The blast crisis (BC) of chronic myeloid leukemia (CML) has poor efficacy against existing treatments and extremely short survival. However, the molecular mechanism CML-chronic phase (CP) transformation to CML-BC is not yet fully understood. Here, we show that Lin28B, an RNA-binding protein, acted as activator enhancing by mediating excessive cell proliferation. level Lin28B expression was apparently elevated in patients with compared newly diagnosed CML-CP. overexpression promoted...

10.1158/1541-7786.mcr-23-0928 article EN Molecular Cancer Research 2024-06-07

<p>Supplementary Figure S5 shows Lin28B-mediated proliferation depends in part on miR-181d K562 and HL60 cells</p>

10.1158/1541-7786.27151031 preprint EN 2024-10-02

<p>Supplementary Figure S1 shows the quantification of immunofluorescence intensity representing Lin28B protein levels by Image J program.</p>

10.1158/1541-7786.27151043 preprint EN 2024-10-02

<p>Supplementary Figure S4 shows the protein level of Lin28A and Lin28B in HEK-293T cell line infected with lentiviruses expressing (Lin28B).</p>

10.1158/1541-7786.27151034 preprint EN 2024-10-02

<p>Supplementary Figure S7 shows the quantification of PDCD4 protein levels detected by Western blot in K562 and HL60 cells transfected with miR-181d mimics or inhibitor their corresponding controls using Image J program, Actin for normalization.</p>

10.1158/1541-7786.27151025 preprint EN 2024-10-02

<p>Supplementary Figure S6 shows schematic illustration of the predicted miR-181d binding site in PDCD4 3’ UTR and specific sequence mutation.</p>

10.1158/1541-7786.27151028 preprint EN 2024-10-02

<p>Supplementary Figure S2 shows shLin28B-1/shLin28B-2 significantly knockdown Lin28B expression in K562 and HL60 cells.</p>

10.1158/1541-7786.27151040 preprint EN 2024-10-02

<p>Supplementary Figure S3 shows schematic illustration of the predicted Lin28B binding sites in miR-181d promoter and specific sequence site mutation.</p>

10.1158/1541-7786.27151037 preprint EN 2024-10-02

<p>Supplementary Figure S8 shows the quantification of Lin28B and PDCD4 protein levels detected by Western blot in stable knockdown K562 HL60 cells relative control transfected with siRNA or NC using Image J program, Actin for normalization.</p>

10.1158/1541-7786.27151022 preprint EN 2024-10-02

<div>Abstract<p>The blast crisis (BC) of chronic myeloid leukemia (CML) has poor efficacy against existing treatments and extremely short survival. However, the molecular mechanism CML-chronic phase (CP) transformation to CML-BC is not yet fully understood. Here, we show that Lin28B, an RNA-binding protein, acted as activator enhancing by mediating excessive cell proliferation. The level Lin28B expression was apparently elevated in patients with compared newly diagnosed CML-CP....

10.1158/1541-7786.c.7476320 preprint EN 2024-10-02

1Blood Purification And Organ Transplantation, Qilu Hospital of Shandong University, Jinan/CHINA, 2Blood Transplatation, 3Terasaki Transplantation Lab, Jinan/CHINA

10.1097/00007890-201007272-01780 article EN Transplantation 2010-07-01
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