Jianmei Hou

ORCID: 0000-0001-7066-5903
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About
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Research Areas
  • Angiogenesis and VEGF in Cancer
  • 14-3-3 protein interactions
  • Microtubule and mitosis dynamics
  • Glycosylation and Glycoproteins Research
  • ATP Synthase and ATPases Research
  • Endoplasmic Reticulum Stress and Disease
  • Virus-based gene therapy research
  • Cell Adhesion Molecules Research
  • Cancer Cells and Metastasis
  • Cancer Research and Treatments
  • PI3K/AKT/mTOR signaling in cancer
  • Immunotherapy and Immune Responses
  • Ubiquitin and proteasome pathways
  • Cancer Genomics and Diagnostics
  • Advanced Proteomics Techniques and Applications
  • Pancreatic function and diabetes
  • HER2/EGFR in Cancer Research
  • interferon and immune responses
  • Cell death mechanisms and regulation
  • Pediatric health and respiratory diseases
  • Histone Deacetylase Inhibitors Research
  • Proteoglycans and glycosaminoglycans research
  • Chemokine receptors and signaling
  • Lung Cancer Research Studies
  • Protein Tyrosine Phosphatases

Monash University
2021-2023

Australian Regenerative Medicine Institute
2021-2023

Guiyang Medical University
2012

Sichuan University
2004-2011

State Key Laboratory of Biotherapy
2009-2011

The Christie NHS Foundation Trust
2011

Cancer Research UK Manchester Institute
2010-2011

University of Manchester
2010

Abstract PEAK pseudokinases regulate cell migration, invasion and proliferation by recruiting key signaling proteins to the cytoskeleton. Despite lacking catalytic activity, alteration in their expression level is associated with several aggressive cancers. Here, we elucidate molecular details of interactions adapter CrkII Grb2 scaffold protein 14-3-3. Our findings rationalize why dimerization has a crucial function signal transduction provide biophysical structural data unravel binding...

10.1038/s41467-023-38869-9 article EN cc-by Nature Communications 2023-06-19

Abstract Purpose: CXC chemokine ligand 10 (CXCL10) is a potent inhibitor of angiogenesis. We wonder whether the combination CXCL10 with cisplatin would improve therapeutic antitumor efficacy. Experiment Design: evaluated activity therapy in immunocompetent C57BL/6 and BALB/c mice bearing LL/2 Lewis lung cancer CT26 colon adenocarcinoma, respectively. Mice were treated either s.c. at 25 μg per kg day once daily for 30 days, cycled twice (5 mg/kg i.p. on days 14 21 after initiation CXCL10), or...

10.1158/1078-0432.ccr-04-2117 article EN Clinical Cancer Research 2005-06-01

The pseudokinase scaffolds PEAK1 and PEAK2 are implicated in cancer cell migration metastasis. We characterized the regulation role of third family member PEAK3 signaling. Similar to PEAK2, formed both homotypic heterotypic complexes. In addition, like PEAK1, it bound adaptors Grb2 CrkII. However, unlike homodimerized also interacted with ARF GTPase-activating protein ASAP1, E3 ubiquitin ligase Cbl, kinase PYK2. Dimerization subsequent phosphorylation on Tyr 24 , likely by a Src kinase, were...

10.1126/scisignal.abj3554 article EN Science Signaling 2022-02-22

Vascular endothelial growth factor receptor-2 (VEGFR-2) has been shown to play a major role in inducing the full spectrum of VEGF biological response which is essential for tumor angiogenesis. We have demonstrated that immunotherapy tumors with vaccine based on quail homologous VEGFR-2 (qVEGFR) was effective providing both protective and therapeutic antitumor immunity several models mice. The purpose this study determine whether combination therapy low-dose gemcitabine qVEGFR as could...

10.1159/000087303 article EN Oncology 2005-01-01

Targeting tumor endothelium is an important strategy for cancer therapy. We evaluated the effectiveness of gene therapy, that is, intramuscular delivery plasmid DNA encoding tumstatin (pSecTag2B-tum), combined with gemcitabine administration in vitro and vivo, using colon carcinoma (CT26) Lewis lung (LLC) murine models. The growth-inhibitory proapoptotic effects and/or on human umbilical vein endothelial cells (HUVECs) mouse (SVEC4-10), respectively, were assessed. vitro, conditioned medium...

10.1089/hum.2005.16.1075 article EN Human Gene Therapy 2005-09-01

In the current study, we investigated whether 17beta-estradiol (E2) induces cyclin E expression and triggers processing via calpain in MCF-7 breast cancer cells. We found that E2 induced increased of a slow persistent manner, rapid yet sustained E. addition, estrogenic ethanol was able to stimulate truncation. Calpeptin or ALLN greatly suppressed E2-triggered its expression, suggesting calpain-mediated action for E2. Finally, E2-induced effects could also be significantly by BAPTA U0126,...

10.1016/j.febslet.2012.02.018 article EN FEBS Letters 2012-02-28

In this study, we used two-dimensional gel electrophoresis and MALDI-Q-TOF-MS/MS analysis to examine the global protein expression of a pair colorectal carcinoma cell lines, SW620 irinotecan-resistant SW620. Of 30 spots identified as differentially expressed proteins (±over twofold, P<0.05) between two 26 (corresponding unique proteins) were positively by analysis. These could be grouped into main classes including metabolism (15.38%), SSproliferation/differentiation (11.53%), molecular...

10.1097/cad.0b013e3283408596 article EN Anti-Cancer Drugs 2011-03-25

BACKGROUND:Chlamydia trachomatis is an obligate intracellular pathogen that can cause severe reproductive tract complications while ascending infection occurs. When spreading from cell to in a host, C. utilizes various survival strategies offset host defense mechanisms. One such strategy degrade antimicrobial proteins before they attack the invading cells. MATERIAL AND METHODS:We expressed and purified recombinant chlamydia high temperature requirement protein A (cHtrA) including 2 cHtrA...

10.12659/msm.923909 article EN Medical Science Monitor 2020-07-07

Abstract The PEAK family of pseudokinases comprises PEAK1 and PEAK2 as well the recently-identified PEAK3. PEAK1/2 play fundamental roles in regulating tyrosine kinase signal output oncogenesis, while PEAK3 remains poorly-characterized. Here, we demonstrate that undergoes homotypic association heterotypic interaction with PEAK1/2. also recruits ASAP1/2, Cbl PYK2 adaptors Grb2 CrkII, binding dependent on dimerization. phosphorylation Y24 is dimerization Src activity, interestingly, decreased...

10.1101/2021.02.17.431740 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-02-19

Abstract PEAK pseudokinases regulate cell migration, invasion and proliferation by recruiting key signaling proteins to the cytoskeleton. Despite lacking catalytic activity, alteration in their expression level is associated with several aggressive cancers. Here, we elucidate new molecular details of interactions adapter CrkII Grb2 scaffold protein 14-3-3. Our findings rationalize why dimerization has a crucial function signal transduction provide biophysical structural data unravel binding...

10.1101/2022.09.01.506260 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-09-02

PEAK pseudokinases (PEAK1, PEAK2 and PEAK3) are important protein scaffolds that regulate cell migration, invasion proliferation by recruiting signalling effectors at the cytoskeleton [1,2].Despite lacking catalytic activity, alteration in expression level of family members is associated with several type aggressive cancers.An emerging thread function ability to utilise homo-and hetero-dimerisation dynamically integrate diversify cellular signals.Our lab was first structurally reveal a...

10.1107/s2053273323086850 article EN Acta Crystallographica Section A Foundations and Advances 2023-08-22

Abstract The PI3-kinase signalling pathway is widely reported to promote survival, proliferation and migration. This up-regulated in several solid tumours by a host of different mechanisms, including PTEN deletion, RAS or PIK3CA mutation aberrant activation receptor tyrosine kinases. As such, inhibitors its down-stream effectors are great interest as tractable anti-cancer agents. effect inhibition was investigated colorectal cancer cell lines demonstrated that, while itself did not cause...

10.1158/1538-7445.am10-1022 article EN Cancer Research 2010-04-01
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