A5051751086- Erythrocyte Function and Pathophysiology
- Cellular transport and secretion
- Chronic Myeloid Leukemia Treatments
- Acute Myeloid Leukemia Research
- Ubiquitin and proteasome pathways
- Hemoglobinopathies and Related Disorders
- PI3K/AKT/mTOR signaling in cancer
- Iron Metabolism and Disorders
- Cancer-related gene regulation
- Protein Kinase Regulation and GTPase Signaling
- Endoplasmic Reticulum Stress and Disease
- Multiple Myeloma Research and Treatments
- Wnt/β-catenin signaling in development and cancer
- Protein Tyrosine Phosphatases
- Blood groups and transfusion
- Histone Deacetylase Inhibitors Research
- Peptidase Inhibition and Analysis
- Prostate Cancer Treatment and Research
- Platelet Disorders and Treatments
- Chronic Lymphocytic Leukemia Research
Biotechnology and Biological Sciences Research Council
2024
Monash University
2011-2021
Babraham Institute
2020
Kymab (United Kingdom)
2019
Abstract INPP4B suppresses PI3K/AKT signaling by converting PI(3,4)P 2 to PI(3)P and inactivation is common in triple-negative breast cancer. Paradoxically, also a reported oncogene other cancers. How these opposing roles relate PI3K regulation unclear. We report PIK3CA -mutant ER + cancers exhibit increased mRNA protein expression the proliferation tumor growth of cancer cells, despite suppression AKT signaling. used integrated proteomics, transcriptomics imaging demonstrate localized late...
Iron plays a major role in the deterioration of β-thalassemia. Indeed, high levels transferrin saturation and iron delivered to erythroid progenitors are associated with production α-globin precipitates that negatively affect erythropoiesis. Matriptase-2/TMPRSS6, membrane-bound serine protease expressed hepatocytes, modulates hepcidin thus is key target prevent overload To address safety concerns raised by suppression Tmprss6 antisense oligonucleotides or small interfering RNA, we tested...
PI3Kγ complexes containing p101 or p84 are directly activated by Gβγ in a GPCR-dependent manner neutrophils.
BACKGROUND Phosphoinositide 3-kinase (PI3K)/Akt pathway is frequently activated in prostate carcinoma due to the loss of tumor suppressor PTEN, which leads increased Akt activity. Expression INPP4B, another negative regulator PI3K/Akt pathway, also reduced carcinoma. However, uncertainty exists regarding association INPP4B expression and biochemical clinical relapse METHODS benign acini was analyzed by co-immunofluorescence with cytokeratins (CK) 5, 8, 19, androgen receptor (AR), c-MET,...
Oncogenic mutations in PIK3CA lead to an increase intrinsic phosphoinositide kinase activity, but it is thought that increased access of PI3Kα (phosphoinositide 3-kinase α) its PM (plasma membrane) localized substrate also required for levels downstream PIP3/Akt [phosphoinositide-3,4,5-trisphosphate/also called PKB (protein B)] signalling. We have studied the subcellular localization wild-type and two most common oncogenic mutants cells maintained growth media, starved or stimulated using a...
Abstract Acute myeloid leukaemia (AML) is an aggressive blood cancer that usually fatal within weeks without effective therapy. Treatment currently involves standard chemotherapy agents such as cytarabine (Ara-C) and anthracyclines but these drugs fail to elicit complete clinical responses in 20-30% of cases. An understanding the mechanisms AML mediating resistance may uncover new oncoproteins amenable medicinal targeting. Activation phosphoinositide 3-kinase (PI3-K)/AKT pathway prevalent...