Ameer L. Elaimy
A5046305055- Vitamin C and Antioxidants Research
- Cancer Research and Treatments
- DNA Repair Mechanisms
- Amino Acid Enzymes and Metabolism
- Glioma Diagnosis and Treatment
- Mitochondrial Function and Pathology
- Biochemical and Molecular Research
- Genomics, phytochemicals, and oxidative stress
- Adenosine and Purinergic Signaling
- PI3K/AKT/mTOR signaling in cancer
- Genetic and Kidney Cyst Diseases
- Cancer, Hypoxia, and Metabolism
- Heat shock proteins research
- GABA and Rice Research
- bioluminescence and chemiluminescence research
- Hepatocellular Carcinoma Treatment and Prognosis
- Histone Deacetylase Inhibitors Research
- Radiation Therapy and Dosimetry
- Epigenetics and DNA Methylation
- Glutathione Transferases and Polymorphisms
- Immune Cell Function and Interaction
- Radiopharmaceutical Chemistry and Applications
- Effects of Radiation Exposure
- Advanced Radiotherapy Techniques
- Metabolism and Genetic Disorders
University of Michigan
2013-2024
Michigan United
2024
University of Newcastle Australia
2019
Junshin Gakuen University
2019
SRM Institute of Science and Technology
2019
Indiana University School of Medicine
2019
Suzuka University of Medical Science
2019
Hospital Infantil de México Federico Gómez
2019
Indiana University – Purdue University Indianapolis
2019
How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links to and has significant therapeutic implications. GTP, but not other nucleotides, the activity of Rac1, guanine nucleotide-binding protein, which promotes dephosphorylation serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, previously known activate repair, nonhomologous end joining. In patients mouse models glioblastoma,...
End-stage liver disease is marked by portal hypertension, systemic elevations in ammonia, and development of hepatocellular carcinoma (HCC). While these clinical consequences cirrhosis are well described, it remains poorly understood whether hepatic insufficiency the accompanying ammonia contribute to HCC carcinogenesis. Using preclinical models, we discovered that entered cell through transporter SLC4A11 served as a nitrogen source for amino acid nucleotide biosynthesis. Elevated promoted...
// Ameer L. Elaimy 1 , Aarif Ahsan Katherine Marsh William B. Pratt 2 Dipankar Ray Theodore S. Lawrence Mukesh K. Nyati Department of Radiation Oncology, The University Michigan Medical School, Ann Arbor, 48109, USA Pharmacology, Correspondence to: Nyati, email: nyati@umich.edu Keywords: Hsp90α, ionizing radiation, γH2AX, ATM, radiosensitization Received: August 26, 2016 Accepted: October 05, Published: 11, ABSTRACT Heat shock protein 90 is a chaperone that plays an essential role in the...
<p>Supplementary Data 1 shows the original data of phosphoproteomic assay in Figure 2.</p>
<p>Supplementary Data 2 shows Supplementary Methods, Reference, Figure S1 and Legends, S2 S3 S4 S5 S6 S7 Legends.</p>
<p>Supplementary Data 2 shows Supplementary Methods, Reference, Figure S1 and Legends, S2 S3 S4 S5 S6 S7 Legends.</p>
<div>ABSTRACT<p>How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links to and has significant therapeutic implications. GTP, but not other nucleotides, the activity of Rac1, guanine nucleotide-binding protein, which promotes dephosphorylation serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, previously known activate repair, nonhomologous end joining. In patients...
<div>ABSTRACT<p>How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links to and has significant therapeutic implications. GTP, but not other nucleotides, the activity of Rac1, guanine nucleotide-binding protein, which promotes dephosphorylation serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, previously known activate repair, nonhomologous end joining. In patients...
<p>Supplementary Data 1 shows the original data of phosphoproteomic assay in Figure 2.</p>
Abstract OBJECTIVE: We sought to define the mechanisms by which purines regulate DNA repair and therapy response. METHODS: Phosphoproteomics was used identify GTP-dependent (de)phosphorylation events after radiation (RT) antibodies generated against novel sites. Animal models of glioblastoma (GBM) normal tissues were assess treatment responses in vivo. RESULTS: Pharmacogenomic inhibition GTP (but not ATP) synthesis sensitized GBM cells RT inhibiting activity non-homologous end joining, but...
Abstract End stage liver disease is marked by portal hypertension, systemic elevations in ammonia, and development of hepatocellular carcinoma (HCC). While these clinical consequences cirrhosis are well described, it remains poorly understood whether hepatic insufficiency the accompanying ammonia contribute to HCC carcinogenesis. Using preclinical models, we discovered that entered cell through transporter SLC4A11 served as a nitrogen source for amino acid nucleotide biosynthesis. Elevated...
Glioblastoma cells preferentially use de-novo purine synthesis pathway, whereas normal brain prefers salvage pathway. Mycophenolate mofetil (MMF), a commonly used oral immunosuppressant that inhibits inosine-5'-monophosphate dehydrogenase (IMPDH), key enzyme in the Pre-clinical suggested MMF can improve radiation and temozolomide efficacy glioblastoma which led to this phase 0/1 trial (NCT04477200) assess MMF's tolerability with chemoradiation glioblastoma, mycophenolic acid accumulation,...
Abstract Glioblastoma prefer de-novo purine synthesis while normal brain prefers resource-efficient salvage pathway. Mycophenolate mofetil (MMF) disrupts metabolism by inhibiting a key enzyme, IMPDH. The pre-clinical evidence of MMF improving radiation and temozolomide efficacy in glioblastoma models led to this first-in-human phase 0/1 trial (NCT04477200) assess the tolerability with chemoradiation glioblastoma, MPA accumulation, inhibition tumor. Tissues from eight 0 recurrent subjects,...
Abstract BACKGROUND Mycophenolate mofetil (MMF) is a commonly used oral immunosuppressant, which exerts its effect by antimetabolite mechanism. Contrary to normal brain preferring salvage purines, resource-efficient, glioblastoma tumor cells prefer make new purine via de-novo pathway. The metabolism can be disrupted using MMF inhibits IMPDH, key enzyme in this There are pre-clinical evidence of improving radiation and temozolomide efficacy mouse models, led first-in-human phase 0/1 trial...
Abstract CD8+ T cells directly target and kill cancer are required for effective antitumor immunity. However, may become dysfunctional when exposed to chronic antigen stimulation during cancer. Dysfunction is characterized by reduced proliferation, increased expression of inhibitory receptors, impaired effector function, yet the genetic mechanisms controlling dysfunction remain poorly understood. To address this gap, we have developed an ex vivo restimulation model that recapitulates...
Abstract Heat-shock protein 90 (Hsp90) is an evolutionary conserved eukaryotic molecular chaperone that has a large number of clients including signaling molecules such as EGFR. Induction Hsp90 upon cellular stress induced by radiation or chemotherapy can enhance stabilization its which may lead to resistance therapy and often provide environment for metastasis. Therefore, targeting been shown be potential therapeutic approach induce EGFR degradation block metastatic spread. The aim this...
How cell metabolism regulates DNA repair is incompletely understood. Here, we define a GTP-mediated signaling cascade that links to and has significant therapeutic implications. GTP, but not other nucleotides, the activity of Rac1, G protein, promotes dephosphorylation serine 323 on Abl-interactor 1 (Abi-1) by protein phosphatase 5 (PP5). Dephosphorylated Abi-1, previously known activate repair, non-homologous end joining. In patients mouse models glioblastoma, Rac1 dephosphorylated Abi-1...
Abstract OBJECTIVE We sought to define the mechanisms by which purines regulate DNA repair and therapy response. METHODS Phosphoproteomics was used identify GTP-dependent (de)phosphorylation events after radiation (RT) antibodies generated against novel sites. Animal models of glioblastoma (GBM) normal tissues were assess treatment responses in vivo. RESULTS Pharmacogenomic inhibition GTP (but not ATP) synthesis sensitized GBM cells RT inhibiting activity non-homologous end joining, but...
Abstract BACKGROUND Mycophenolate mofetil (MMF), a purine synthesis inhibitor, improves radiation and temozolomide efficacy in preclinical glioblastoma models. This phase 0/1 trial (NCT04477200) is the first-in-human study to assess tolerability of MMF with chemoradiation glioblastoma, MPA accumulation, inhibition tumor. METHODS Adult patients meeting eligibility are given 500-2000 PO BID using TITE-CRM dose assignment. Thirty recurrent receive one-week prior concurrently re-irradiation...