Theresa Tachie-Menson

ORCID: 0000-0003-0872-4030
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About
Contact & Profiles
Research Areas
  • Dermatology and Skin Diseases
  • S100 Proteins and Annexins
  • Wnt/β-catenin signaling in development and cancer
  • Genetics, Aging, and Longevity in Model Organisms
  • Asthma and respiratory diseases
  • Bone and Dental Protein Studies
  • Skin and Cellular Biology Research
  • Hippo pathway signaling and YAP/TAZ
  • Endoplasmic Reticulum Stress and Disease
  • Cancer Research and Treatments
  • thermodynamics and calorimetric analyses
  • Insect Resistance and Genetics
  • Redox biology and oxidative stress
  • Pharmacological Effects of Natural Compounds
  • Mass Spectrometry Techniques and Applications
  • Bee Products Chemical Analysis
  • Ubiquitin and proteasome pathways
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Urticaria and Related Conditions
  • Receptor Mechanisms and Signaling
  • Signaling Pathways in Disease
  • Cellular transport and secretion
  • Retinal Development and Disorders
  • Biotin and Related Studies

Queen Mary University of London
2023-2024

Institute of Child Health
2024

University College London
2024

University of Dundee
2017-2020

MRC Protein Phosphorylation and Ubiquitylation Unit
2018-2020

Medical Research Council
2018-2020

University of Liverpool
2020

St George's, University of London
2016-2017

Oxidative stress is linked to many pathological conditions including the loss of dopaminergic neurons in Parkinson's disease. The vast majority disease cases appear be caused by a combination genetic mutations and environmental factors. We screened for genes protecting Caenorhabditis elegans from oxidative induced neurotoxin 6-hydroxydopamine (6-OHDA) identified transthyretin-related gene ttr-33. only described C. protein date, TTR-52, has been shown mediate corpse engulfment as well axon...

10.1371/journal.pgen.1007125 article EN cc-by PLoS Genetics 2018-01-18

<ns4:p><ns4:bold>Background:</ns4:bold> Two recessive mutations in the <ns4:italic>FAM83G</ns4:italic> gene, causing A34E and R52P amino acid substitutions DUF1669 domain of PAWS1 protein, are associated with palmoplantar keratoderma (PPK) humans dogs respectively. We have previously reported that associates Ser/Thr protein kinase CK1α through to mediate canonical Wnt signalling.</ns4:p><ns4:p> <ns4:bold>Methods:</ns4:bold> Co-immunoprecipitation was used investigate possible changes...

10.12688/wellcomeopenres.15403.1 preprint EN cc-by Wellcome Open Research 2019-09-09

The majority of mutations identified in patients with amelogenesis imperfecta have been mapped to FAM83H. As FAM83H expression is not limited the enamel, how contributes still largely unknown. We previously reported that members FAM83 family proteins interact and regulate subcellular distribution promiscuous serine-threonine protein kinase CK1 family, through their shared N-terminal DUF1669 domains. co-localises isoforms speckle-like structures both cytoplasm nucleus. In this report, we show...

10.1016/j.cellsig.2020.109632 article EN cc-by Cellular Signalling 2020-04-11

<ns4:p><ns4:bold>Background:</ns4:bold> Two recessive mutations in the <ns4:italic>FAM83G</ns4:italic> gene, causing A34E and R52P amino acid substitutions DUF1669 domain of PAWS1 protein, are associated with palmoplantar keratoderma (PPK) humans dogs respectively. We have previously reported that associates Ser/Thr protein kinase CK1α through to mediate canonical Wnt signalling.</ns4:p><ns4:p> <ns4:bold>Methods:</ns4:bold> Co-immunoprecipitation was used investigate possible changes...

10.12688/wellcomeopenres.15403.2 preprint EN cc-by Wellcome Open Research 2020-02-17

Abstract Atopic eczema (AE) is the most common inflammatory dermatosis, affecting up to 20% of children. Loss function mutations in Filaggrin ( FLG ) gene are strongly implicated genetic risk factor for AE, but little known about signalling pathways altered response loss FLG. To explore downstream effects on cellular environment, we combined RNAseq analysis siRNA knockdown normal human keratinocytes and tape strip (TS) samples from AE patients who were clinically phenotyped genotyped...

10.1101/2024.03.11.584344 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-03-12

Abstract Introduction and aims Atopic dermatitis (AD) is a chronic skin condition ranked the 15th highest global burden for all nonfatal diseases. Our lab has found that patients with AD have reduction in gene protein expression of cathepsin H, lysosomal cysteine protease aminopeptidase activity. Ctsh-/- mice reduced integrity epidermal barrier, including filaggrin processing, corneocyte change several proinflammatory mediators interleukin-1α. We aim to elucidate roles H keratinocytes...

10.1093/bjd/ljae105.037 article EN British Journal of Dermatology 2024-05-17

Abstract Atopic dermatitis (AD) is a persisting skin condition characterized by recurring eczematous lesions and pruritus. It ranked as nonfatal disease with the fifteenth-highest global burden. The causes of AD are diverse: defective epidermal barrier, inflammation, an altered microbiome genetics. However, much treatment for focuses on reducing inflammation. Further understanding how barrier maintains its integrity may be useful in developing treatments that specifically help to restore...

10.1093/bjd/ljad174.048 article EN British Journal of Dermatology 2023-07-01

Abstract Oxidative stress is linked to many pathological conditions including the loss of dopaminergic neurons in Parkinson’s disease. The vast majority disease cases appear be caused by a combination genetic mutations and environmental factors. We screened for genes protecting Caenorhabditis elegans from oxidative induced neurotoxin 6-hydroxydopamine (6-OHDA) identified t rans hyretin- r elated gene ttr-33. only described C. transthyretin-related protein date, TTR-52, has been shown mediate...

10.1101/198606 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2017-10-13
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