Miranda Machacek

ORCID: 0000-0003-1067-0561
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About
Contact & Profiles
Research Areas
  • Glycosylation and Glycoproteins Research
  • Galectins and Cancer Biology
  • Carbohydrate Chemistry and Synthesis
  • Immune Cell Function and Interaction
  • Polyamine Metabolism and Applications
  • Protein Tyrosine Phosphatases
  • Renal cell carcinoma treatment
  • Metabolomics and Mass Spectrometry Studies
  • Bladder and Urothelial Cancer Treatments
  • Leptospirosis research and findings
  • Polyomavirus and related diseases
  • Urinary and Genital Oncology Studies
  • Spinal Dysraphism and Malformations
  • Tuberous Sclerosis Complex Research
  • Microbial Metabolic Engineering and Bioproduction
  • Epigenetics and DNA Methylation
  • Microtubule and mitosis dynamics
  • Plant biochemistry and biosynthesis
  • Helicobacter pylori-related gastroenterology studies
  • Neurogenetic and Muscular Disorders Research
  • Barrier Structure and Function Studies
  • Amoebic Infections and Treatments
  • T-cell and Retrovirus Studies
  • Monoclonal and Polyclonal Antibodies Research
  • Cytokine Signaling Pathways and Interactions

Massachusetts General Hospital
2020-2024

Harvard University
2024

Centers for Disease Control and Prevention
2024

University of Kansas Medical Center
2016-2020

University of Kansas
2016

R&D Systems (United States)
2010-2014

Boston University
2009

A nonradioactive glycosyltransferase assay is described here. This method takes advantage of specific phosphatases that can be added into reactions to quantitatively release inorganic phosphate from the leaving groups reactions. The released group then detected using colorimetric malachite-based reagents. Because amount directly proportional sugar molecule transferred in a reaction, this used obtain accurate kinetic parameters glycosyltransferase. performed multiwell plates and quantitated...

10.1093/glycob/cwq187 article EN Glycobiology 2010-11-15

Chronic, low-grade inflammation increases the risk for atherosclerosis, cancer, and autoimmunity in diseases such as obesity diabetes. Levels of CD4+ T helper 17 (Th17) cells, which secrete interleukin 17A (IL-17A), are increased contribute to inflammatory milieu; however, relationship between signaling events triggered by excess nutrient levels IL-17A–mediated is unclear. Here, using cytokine, quantitative real-time PCR, immunoprecipitation, ChIP assays, along with lipidomics MS-based...

10.1074/jbc.ra119.008373 article EN cc-by Journal of Biological Chemistry 2019-04-22

Alterations in O-GlcNAc cycling, the addition and removal of O-GlcNAc, lead to mitotic defects increased aneuploidy. Herein, we generated stable O-GlcNAcase (OGA, enzyme that removes O-GlcNAc) knockdown HeLa cell lines characterized effect reduction OGA activity on cycle progression. After release from G1/S, cells progressed normally through S phase but demonstrated exit defects. Cyclin A was while B D expression reduced. Retinoblastoma protein (RB) phosphorylation also compared control. At...

10.1080/15384101.2016.1167297 article EN Cell Cycle 2016-04-12

A 37-year-old man was transferred to the hospital because of fever, myalgia, and hypoxemia. Evaluation revealed leukocytosis, acute kidney failure, conjugated hyperbilirubinemia. diagnosis made.

10.1056/nejmcpc2402493 article EN New England Journal of Medicine 2024-10-09

This communication explores prenyltransferase substrate binding pocket flexibility to tag and enrich isoprenoids using affinity-based purification for metabolomic studies.

10.1039/b902370d article EN Molecular BioSystems 2009-01-01

Staging of renal pelvic urothelial carcinoma can be challenging due to anatomic variation at the pelvis compared with ureter and bladder calls into question prognostic accuracy current TNM staging. In this study, we determined staging cancer-specific survival (CSS) in 141 patients undergoing nephroureterectomy for (pTa=50, pT1=29, pT2=10, pT3=36, pT4=16). Under criteria, found no significant difference CSS between adjacent categories step-wise across pTa, pT1, pT2, pT3 tumors. When tumors...

10.1097/pas.0000000000002331 article EN The American Journal of Surgical Pathology 2024-11-14

SUMMARY Chronic, low-grade inflammation increases the risk of atherosclerosis, cancer, and autoimmunity in diseases like obesity diabetes. Here, we show that increased levels nutrient-responsive, post-translational protein modification, O-GlcNAc (O-linked β-N-acetylglucosamine) are present naïve CD4+ T cells from a diet-induced murine model, elevation leads to pro-inflammatory IL-17A production. Importantly, helper 17 (Th17) cells, which secrete IL-17A, contribute inflammatory milieu. We...

10.1101/305722 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-04-20

Abstract Chronic inflammation is a feature of diabetes and obesity enhances the risk atherosclerosis cancer. Specifically, proinflammatory Th1 Th17 CD4+ T cells are increased in metabolic diseases. However, clear molecular mechanism linking changes with lacking. We hypothesize that elevated levels O-linked β-N-acetylglucosamine (O-GlcNAc), post-translational modification nuclear cytoplasmic proteins, promotes cell differentiation. Since production O-GlcNAc involves input from carbohydrate,...

10.4049/jimmunol.196.supp.133.22 article EN The Journal of Immunology 2016-05-01

Effector CD4+ T cells (i.e. Th1, Th2, Th17) are essential in the adaptive immune system’s specific elimination of different classes pathogens, such as viruses, bacteria, and parasites, while regulatory shut these inflammatory responses off once a pathogen has been cleared

10.33696/immunology.2.028 article EN cc-by Journal of Cellular Immunology 2020-06-26

In a normal immune response, antigen presenting cells (APC) engage the T cell receptor on CD4+ cells, stimulating proliferation and inducing differentiation in conjunction with cytokines secreted by APC. differentiate into effectors which secrete able to specifically neutralize different classes of pathogens. Pro‐inflammatory Th1 Th17 effector are known increase situations altered metabolism, such as type 1 2 diabetes inflammatory bowel disease. A clear mechanism linking metabolic changes...

10.1096/fasebj.30.1_supplement.652.6 article EN The FASEB Journal 2016-04-01

Abstract Chronic inflammation is a feature of obesity and enhances the risk heart disease, cancer, diabetes. Specifically, pro-inflammatory TH1 TH17 CD4+ effector T cells are increased in metabolic diseases. However, clear molecular mechanism linking changes with lacking. We hypothesize that elevated levels O-linked β-N-acetylglucosamine (O-GlcNAc), post-translational modification (PTM) nuclear cytoplasmic proteins, promotes cell differentiation. Since production O-GlcNAc involves input from...

10.4049/jimmunol.198.supp.223.9 article EN The Journal of Immunology 2017-05-01

O‐linked N ‐acetylglucosamine (O‐GlcNAc) is the attachment of a single β‐N‐acetylglucosamine to serine/threonine amino acid residues nuclear, cytoplasmic, and mitochondrial proteins. The modification sensitive changes in cellular environment dynamically regulated by opposing functions two specific enzymes; O‐GlcNAc transferase (OGT) adds modification, whereas, O‐GlcNAcase (OGA) removes it. Disruptions cycling contribute diseases such as neurodegeneration. Dysfunctional mitochondria lead...

10.1096/fasebj.31.1_supplement.778.8 article EN The FASEB Journal 2017-04-01

Chronic inflammation is a feature of obesity and enhances the risk atherosclerosis, cancer, diabetes, autoimmunity. Specifically, pro-inflammatory TH17 CD4+ effector T cells are increased in metabolic diseases. However, clear molecular mechanism linking changes with lacking. We hypothesize that elevated levels O-linked β-N-acetylglucosamine (O-GlcNAc), post-translational modification nuclear cytoplasmic proteins, promotes cell function. Since production O-GlcNAc involves input from...

10.1096/fasebj.2018.32.1_supplement.673.9 article EN The FASEB Journal 2018-04-01
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