Characterization of tweety gene (ttyh1-3) expression in Xenopus laevis during embryonic development

Halleran, Andrew D.; Sehdev, Morgan; Rabe, Brian; Huyck, Ryan W.; Williams, Cheyenne C.; Saha, Margaret S.

doi:10.1016/j.gep.2014.12.002

Cited by 27 publications

(30 citation statements)

References 36 publications

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“…TTYH3 belongs to the tweety family of genes encoding large-conductance chloride channels and are implicated in a wide array of cellular processes, such as cell division, cell adhesion, regulation of calcium activity, and tumorigenesis, particularly in neuronal cells throughout embryonic development [16]. GNA12 has been shown to be involved in human pancreatic adenocarcinoma cell migration, hepatocarcinoma progression, and oral squamous cell carcinoma invasion, and may play a role in the pathogenesis of pre-eclampsia [17–20].…”

Section: Discussionmentioning

confidence: 99%

Rare copy number variants in the genome of Chinese female children and adolescents with Turner syndrome

Wang

et al. 2019

Bioscience Reports

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Turner syndrome (TS) is a congenital disease caused by complete or partial loss of one X chromosome. Low bone mineral status is a major phenotypic characteristic of TS that can not be fully explained by X chromosome loss, suggesting other autosomal-linked mutations may also exist. Therefore, the present study aimed to detect potential genetic mutations in TS through examination of copy number variation (CNV). Seventeen patients with TS and 15 healthy volunteer girls were recruited. Array-based comparative genomic hybridization (a-CGH) was performed on whole blood genomic DNA (gDMA) from the 17 TS patients and 15 healthy volunteer girls to identify potential CNVs. The abnormal CNV of one identified gene (CARD11) was verified by quantitative PCR. All cases diagnosed had TS based on genotype examination and physical characteristics, including short stature and premature ovarian failure. Three rare CNVs, located individually at 7p22.3, 7p22.2, and Xp22.33, where six genes (TTYH3, AMZ1, GNA12, BC038729, CARD11, and SHOX (stature homeobox)) are located, were found in TS patients. Quantitative PCR confirmed the CNV of CARD11 in the genome of TS patients. Our results indicate that CARD11 gene is one of the mutated genes involved in TS disease. However, this CNV is rare and its contribution to TS phenotype requires further study.

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Section: Discussionmentioning

confidence: 99%

Rare copy number variants in the genome of Chinese female children and adolescents with Turner syndrome

Wang

et al. 2019

Bioscience Reports

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“…TTYH3 (Tweety Family Member 3) encodes for a large‐conductance chloride channel (Suzuki & Mizuno, ). In Xenopus laevis , ttyh3 is expressed during embryonic development in the nervous system and in somites (Halleran et al, ). It is not yet known whether there is similar expression in humans.…”

Section: Discussionmentioning

confidence: 99%

Variable developmental delays and characteristic facial features—A novel 7p22.3p22.2 microdeletion syndrome?

Zambrano

Cristian

et al. 2017

American J of Med Genetics Pt A

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Isolated 7p22.3p22.2 deletions are rarely described with only two reports in the literature. Most other reported cases either involve a much larger region of the 7p arm or have an additional copy number variation. Here, we report five patients with overlapping microdeletions at 7p22.3p22.2. The patients presented with variable developmental delays, exhibiting relative weaknesses in expressive language skills and relative strengths in gross, and fine motor skills. The most consistent facial features seen in these patients included a broad nasal root, a prominent forehead a prominent glabella and arched eyebrows. Additional variable features amongst the patients included microcephaly, metopic ridging or craniosynostosis, cleft palate, cardiac defects, and mild hypotonia. Although the patients' deletions varied in size, there was a 0.47 Mb region of overlap which contained 7 OMIM genes: EIP3B, CHST12, LFNG, BRAT1, TTYH3, AMZ1, and GNA12. We propose that monosomy of this region represents a novel microdeletion syndrome. We recommend that individuals with 7p22.3p22.2 deletions should receive a developmental assessment and a thorough cardiac exam, with consideration of an echocardiogram, as part of their initial evaluation.

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“…The tweety family of genes (TTYHs) is reported as chloride channel responsive genes and has been contributing in several cellular processes including cell adhesion, cell division, tumorigenesis, and regulation of calcium activity [13]. The TTYH1 gene, the first member of the TTYHs, encodes a protein that forms swelling-activated chloride ion channels [14].…”

Section: Introductionmentioning

confidence: 99%

High Expression of TTYH3 Is Related to Poor Clinical Outcomes in Human Gastric Cancer

Saha

Biswas

Gil

et al. 2019

JCM

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Ion channels play important roles in regulating various cellular processes and malignant transformation. Expressions of some chloride channels have been suggested to be associated with patient survival in gastric cancer (GC). However, little is known about the expression and function of TTYH3, a gene encoding a chloride ion channel, in cancer progression. Here, we comprehensively analyzed the expression of TTYH3 and its clinical outcome in GC using publicly available cancer gene expression and patient survival data through various databases. We examined the differences of TTYH3 expression between cancers and their normal tissues using the Oncomine, UALCAN, and GEO (Gene Expression Omnibus) databases. TTYH3 expression was investigated from immunohistochemistry images using the Human Protein Atlas database. Copy number alterations and mutations of TTYH3 were analyzed using cBioPortal. The co-expression profile of TTYH3 in GC was revealed using Oncomine. The gene ontology and pathway analyses were done using those co-expressed genes via the Enrichr tool to explore the predicted signaling pathways in GC. TTYH3 mRNA and protein levels in GC were significantly greater than those in normal tissue. Kaplan–Meier analysis revealed the upregulation of TTYH3 expression, which was significantly correlated with worse patient survival. Collectively, our data suggest that TTYH3 might be a potential prognostic marker for GC patients.

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Characterization of tweety gene (ttyh1-3) expression in Xenopus laevis during embryonic development

Cited by 27 publications

References 36 publications

Rare copy number variants in the genome of Chinese female children and adolescents with Turner syndrome

Rare copy number variants in the genome of Chinese female children and adolescents with Turner syndrome

Variable developmental delays and characteristic facial features—A novel 7p22.3p22.2 microdeletion syndrome?

High Expression of TTYH3 Is Related to Poor Clinical Outcomes in Human Gastric Cancer

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