Publications by authors named "K Al-Zahrani"

Highly mutable pathogens generate viral diversity that impacts virulence, transmissibility, treatment, and thwarts acquired immunity. We previously described C19-SPAR-Seq, a high-throughput, next-generation sequencing platform to detect SARS-CoV-2 that we here deployed to systematically profile variant dynamics of SARS-CoV-2 for over 3 years in a large, North American urban environment (Toronto, Canada). Sequencing of the ACE2 receptor binding motif and polybasic furin cleavage site of the Spike gene in over 70,000 patients revealed that population sweeps of canonical variants of concern (VOCs) occurred in repeating wavelets.

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Background The prevalence of obesity has increased over the years, resulting in multiple physical and psychological health issues that impact the quality of human life. Numerous Western studies have linked obesity and depression, but few studies have investigated this correlation among the Saudi population. Hence, this study assesses the correlation between obesity and depression among the general population of Saudi Arabia.

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Aims: To determine the acceptability and identify potential concerns and barriers of using a hypothetical smartphone application (app) for home monitoring (HM) of visual function among patients with diabetes.

Methods: Quantitative, cross-sectional study using a self-administered questionnaire. Patients diagnosed with diabetes aged between 20 and 70 years were included.

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Functionally characterizing the genetic alterations that drive pancreatic cancer is a prerequisite for precision medicine. Here, we perform somatic CRISPR/Cas9 mutagenesis screens to assess the transforming potential of 125 recurrently mutated pancreatic cancer genes, which revealed USP15 and SCAF1 as pancreatic tumor suppressors. Mechanistically, we find that USP15 functions in a haploinsufficient manner and that loss of USP15 or SCAF1 leads to reduced inflammatory TNFα, TGF-β and IL6 responses and increased sensitivity to PARP inhibition and Gemcitabine.

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Article Synopsis
  • Tumor suppressor p53 (TP53) mutations in cancer lead to loss of its protective function and potential gain of oncogenic traits, with mutant forms often stabilized in tumors.
  • Researchers conducted CRISPR screens to identify factors that regulate the stability of wild-type and mutant p53, revealing that most regulators affect both, but some, like those for mutant p53 R337H, are specific to that mutant.
  • The study highlights FBXO42 as a positive regulator for certain p53 mutants and C16orf72/HAPSTR1 as a negative regulator linked to increased levels in breast cancer, suggesting potential targets for cancer therapy focused on p53 stability.
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