Huda A BinEssa
16 Papers
12 Citations
Huda A BinEssa is an academic researcher. The author has contributed to research in topics: Mutation & Biology. The author has an hindex of 7, co-authored 15 publications.
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Papers
Molecular Analysis of Congenital Hypothyroidism in Saudi Arabia: SLC26A7 Mutation Is a Novel Defect in Thyroid Dyshormonogenesis.
Minjing Zou,Ali S. Alzahrani,Ali Al-Odaib,Mohammad A. Alqahtani,Omer Babiker,Roua A. Al-Rijjal,Huda A BinEssa,Walaa E Kattan,Anwar F Al-Enezi,Ali Al Qarni,Manar S A Al-Faham,Essa Y. Baitei,Afaf Alsagheir,Brian F. Meyer,Yufei Shi +14 more
TL;DR: TG and TSHR mutations are the most common genetic defects in Saudi patients with CH and the prevalence of other disease-causing mutations is low, reflecting the consanguineous nature of the population.
TSH overcomes Braf(V600E)-induced senescence to promote tumor progression via downregulation of p53 expression in papillary thyroid cancer.
Minjing Zou,Essa Y. Baitei,Roua A. Al-Rijjal,Ranjit S. Parhar,Futwan Al-Mohanna,Shioko Kimura,Catrin Pritchard,Huda A BinEssa,Ali S. Alzahrani,H H Al-Khalaf,A Hawwari,Mohammed Akhtar,Abdullah Mohammed Assiri,Brian F. Meyer,Yufei Shi +14 more
TL;DR: BVE–PTC progression could be contained via p53-dependent OIS and TSH is a major disruptor of this balance, and simultaneous targeting of both MAPK and PI3K/AKT pathways offer a better therapeutic outcome against ATC.
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Mutational analysis of PHEX, FGF23 and CLCN5 in patients with hypophosphataemic rickets
Ayla Güven,Roua A. Al-Rijjal,Huda A BinEssa,Durmuş Doğan,Yılmaz Kor,Minjing Zou,Namik Kaya,Anwar F Al-Enezi,Suna Hancili,Ömer Tarım,Essa Y. Baitei,Walaa E Kattan,Brian F. Meyer,Yufei Shi +13 more
TL;DR: Hypophosphataemic rickets is a group of rare hereditary renal phosphate wasting disorders caused by mutations in PHEX, FGF23, DMP1, ENPP1, CLCN5 or SLC34A3.
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Functional analysis of 22 splice-site mutations in the PHEX, the causative gene in X-linked dominant hypophosphatemic rickets
Huda A BinEssa,Minjing Zou,Anwar F Al-Enezi,Basma Alomrani,Manar S A Al-Faham,Roua A. Al-Rijjal,Brian F. Meyer,Yufei Shi +7 more
TL;DR: Exon skipping is the most common outcome due to splice-site mutations, resulting in incomplete inactivation of PHEX gene, which may explain the mild disease phenotype reported previously, providing evidence of genotype-phenotype correlation.
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Cyp24a1 Attenuation Limits Progression of BrafV600E -Induced Papillary Thyroid Cancer Cells and Sensitizes Them to BRAFV600E Inhibitor PLX4720.
Minjing Zou,Essa Y. Baitei,Huda A BinEssa,Futwan Al-Mohanna,Ranjit S. Parhar,René St-Arnaud,Shioko Kimura,Catrin Pritchard,Ali S. Alzahrani,Abdullah Mohammed Assiri,Brian F. Meyer,Yufei Shi +11 more
TL;DR: These findings offer direct evidence that Cyp24a1 functions as an oncogene in PTC, where its overexpression activates multiple signaling cascades to promote malignant progression and resistance to PLX4720 treatment.