Zhenxi Li (0000-0002-7220-6177)

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Biography

Zhenxi Li received the B.S. degree in Biological Science from Henan Normal University, Henan, China, in 2007 and the Ph.D. degree in Biomedical Science from East China Normal University, Shanghai, China, in 2012. She worked in Shanghai Changzheng Hospital from 2012.9 to 2022.10. She is woking in University of Shanghai for Science and Technology. She is an associated professor. Her research interests include bone diseases, GPCR signal transduction and protein post-translational modification.

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University of Shanghai for Science and Technology: Shanghai, CN

2022-11 to present | professor (Institute of Biomedical Sciences and Clinical Technology Transformation)

Employment

Zhenxi Li

https://orcid.org/0000-0002-7220-6177

Personal information

Biography

Activities

Employment (2)

University of Shanghai for Science and Technology: Shanghai, CN

Shanghai Changzheng Hospital: Shanghai, Shanghai, CN

Education and qualifications (6)

University of Shanghai for Science and Technology: Shanghai, CN

Shanghai Changzheng Hospital Department of Orthopaedic: Shanghai, CN

Harvard Medical School: Boston, MA, US

Shanghai Changzheng Hospital Department of Orthopaedic: Shanghai, CN

East China Normal University: Shanghai, Shanghai, CN

Henan Normal University: Henan, CN

Funding (6)

Molecular mechanism of Tamoxifen resistance in ER+ breast Cancer induced by integration of metabolic reprogramming and epigenetic modification

Study on the effect and mechanism of C5a/C5aRs regulating PD-L1 and OPN in promoting immune escape and bone injury of breast cancer in the bone marrow microenvironment

Effect of betulinic acid derivatives on osteoporosis and its molecular mechanism

Regulation of bone metabolism by bile acid /Tgr5 and its mechanism

Targeting Tgr5 in the treatment of bone metabolic diseases and its mechanism

Function and mechanism of Gpr54 in osteoclasts

Works (25)

Author Correction: Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src

Predictive Value of Preoperative Serum Albumin in Patients With Metastatic Spine Diseases: A Statistical Comment

Kisspeptin-10 binding to Gpr54 in osteoclasts prevents bone loss by activating Dusp18-mediated dephosphorylation of Src

Roles of calcium signaling in cancer metastasis to bone.

Functional analysis of the emerging roles for the KISS1/KISS1R signaling pathway in cancer metastasis

RSPO2 and RANKL signal through LGR4 to regulate osteoclastic premetastatic niche formation and bone metastasis.

Kiss1/Gpr54 Prevents Bone Loss through Src Dephosphorylation by Dusp18 in Osteoclasts

KP-10/Gpr54 attenuates rheumatic arthritis through inactivating NF-κB and MAPK signaling in macrophages

Whole Genome Sequencing Identifies Key Genes in Spinal Schwannoma.

Apatinib in patients with advanced chordoma: a single-arm, single-centre, phase 2 study.

NAT1 promotes osteolytic metastasis in luminal breast cancer by regulating the bone metastatic niche via NF-κB/IL-1B signaling pathway.

Regulation of body length and bone mass by Gpr126/Adgrg6.

Stromal Cell-Derived CCL20 Promotes Tumor Progression and Osteolysis in Giant Cell Tumor of Bone

Dual Targeting of Bile Acid Receptor‐1 (TGR5) and Farnesoid X Receptor (FXR) Prevents Estrogen‐Dependent Bone Loss in Mice

NPNT promotes early-stage bone metastases in breast cancer by regulation of the osteogenic niche.

Outcomes and prognostic factors for surgically treated patients with breast cancer spine metastases.

TGF-β induced PAR-1 expression promotes tumor progression and osteoclast differentiation in giant cell tumor of bone.

5-Fluoruracil blocked giant cell tumor progression by suppressing osteoclastogenesis through NF-kappaB signals and blocking angiogenesis.

MiR-30a inhibits osteolysis by targeting RunX2 in giant cell tumor of bone.

GPR116, an adhesion G-protein-coupled receptor, promotes breast cancer metastasis via the Gαq-p63RhoGEF-Rho GTPase pathway.

Inhibition of breast cancer metastases by a novel inhibitor of TGFβ receptor 1.

Synthesis and Biological Evaluation of Heterocyclic Ring-Fused Betulinic Acid Derivatives as Novel Inhibitors of Osteoclast Differentiation and Bone Resorption

Nitidine Chloride inhibits breast cancer cells migration and invasion by suppressing c-Src/FAK associated signaling pathway.

Maslinic acid suppresses osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-mediated NF-κB and MAPK signaling pathways.