Publications by authors named "Thiago Milech de Assuncao"

Current capabilities in genomic sequencing outpace functional interpretations. Our previous work showed that 3D protein structure calculations enhance mechanistic understanding of genetic variation in sequenced tumors and patients with rare diseases. The KRAS GTPase is among the critical genetic factors driving cancer and germline conditions.

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Current capabilities in genomic sequencing outpace functional interpretations. Our previous work showed that 3D protein structure calculations enhance mechanistic understanding of genetic variation in sequenced tumors and patients with rare diseases. The KRAS GTPase is among the critical genetic factors driving cancer and germline conditions.

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Article Synopsis
  • Kras mutations are the main cause of pancreatic ductal adenocarcinoma initiation and can be studied using GEMM-derived cell models with inducible Kras expression.
  • The study examines how the transcriptional response to Kras activation involves mainly downregulated gene expression and correlates with epigenetic changes, particularly chromatin remodeling.
  • The findings reveal a detailed early epigenomic program regulated by Kras that is crucial for understanding the transcriptional activity associated with this oncogene in pancreatic cells.*
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Article Synopsis
  • Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a low 5-year survival rate, and recent studies have highlighted the importance of epigenomic changes, particularly the H3K9me pathway, in its progression.
  • The enzyme EHMT2, responsible for producing H3K9me, acts as a crucial mediator of oncogenic KRAS during both PDAC initiation and inflammation-related promotion, with its inactivation showing potential to hinder tumor growth in models.
  • Findings indicate that EHMT2's role includes enhancing cancer cell senescence and lowering inflammatory responses associated with KRAS-driven tumor processes, underlining a significant KRAS-EHMT2 interaction in PDAC pathology.
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Objectives: To determine the potential of bi-parametric dual-frequency hepatic MR elastography (MRE) for predicting portal pressure (PP) in mouse models of portal hypertension (PHTN) with the presence of varying hepatic fibrosis.

Methods: We studied 73 wild-type male mice, including 22 mice with hepatic congestion, 20 mice with cholestatic liver injury, and 31 age-matched sham mice. Hepatic shear stiffness (SS) and volumetric strain (VS) were calculated by 3D MRE acquired at 80 and 200 Hz.

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By reading the H3K9Me3 mark through their N-terminal chromodomain (CD), HP1 proteins play a significant role in cancer-associated processes, including cell proliferation, differentiation, chromosomal stability, and DNA repair. Here, we used a combination of bioinformatics-based methodologies, as well as experimentally-derived datasets, that reveal the existence of a novel short HP1γ (CBX3) isoform, named here sHP1γ, generated by alternative splicing of the CBX3 locus. The sHP1γ mRNA encodes a protein composed of 101 residues and lacks the C-terminal chromoshadow domain (CSD) that is required for dimerization and heterodimerization in the previously described 183 a.

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The scaffold protein synectin plays a critical role in the trafficking and regulation of membrane receptor pathways. As platelet-derived growth factor receptor (PDGFR) is essential for hepatic stellate cell (HSC) activation and liver fibrosis, we sought to determine the role of synectin on the PDGFR pathway and development of liver fibrosis. Mice with deletion of synectin from HSC were found to be protected from liver fibrosis.

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Diagnostic methods of TB, nowadays, are prone to delay in diagnosis, increased false negative results and are not sensitive to many forms of paucibacillary disease. The aims of this study were to implement a quantitative nucleic acid-based diagnostic test for paucibacillary tuberculosis, enabling the identification and quantification of viable Mycobacterium tuberculosis bacilli by quantitative Real-Time PCR (qRT-PCR). The intergenic region of the single-copy inhA-mabA gene was chosen as the target region for design of primers and probes conjugated with fluorophores.

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Purine nucleoside phosphorylase (PNP) is a purine-metabolizing enzyme that catalyzes the reversible phosphorolysis of 6-oxypurine (deoxy)nucleosides to their respective bases and (deoxy)ribose-1-phosphate. It is a key enzyme in the purine salvage pathway of mammalian cells. The present investigation sought to determine whether the PNP transition state analog inhibitor (Immucillin-H) arrests bone loss in two models of induced periodontal disease in rats.

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