0.2 ml Flat Cap PCR Tube
- Known as:
- 0.2 milliliter Flat Cap PCR test kit Tube
- Catalog number:
- TC2-02-B
- Product Quantity:
- 1000 ea
- Category:
- -
- Supplier:
- Bioner
- Gene target:
- 0.2 Flat Cap PCR Tube
Related genes to: 0.2 ml Flat Cap PCR Tube
- Gene:
- CFAP126 NIH gene
- Name:
- cilia and flagella associated protein 126
- Previous symbol:
- C1orf192
- Synonyms:
- Flattop, Fltp
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-11
- Date modifiied:
- 2014-11-19
Related products to: 0.2 ml Flat Cap PCR Tube
Related articles to: 0.2 ml Flat Cap PCR Tube
- Deriving functional β-cells from human induced pluripotent stem cells (hiPSCs) holds potential for cell replacement therapy, disease modeling, and drug testing in diabetes research. Wnt/Planar cell polarity (PCP) signaling is crucial for endocrine cell development and β-cell maturation in murine models and can be tracked by the expression of the tissue-specific effector gene Flattop. Here, we report the generation of a human fluorescent FLTP/CFAP126 (Flattop-T2A-H2B-Venus) and FLTP-Insulin (Flattop-T2A-H2B-Venus x C-peptide-mCherry) double reporter by CRISPR/Cas9 gene editing. These hiPSC reporter lines allow monitoring of WNT/PCP signaling during endocrine cell formation and studying its role in β-cells in a human model system. - Source: PubMed
Publication date: 2025/09/19
Greisle TobiasKunze InesWang XianmingMalinowski Andrzej RBöttcher AnikaLickert HeikoBurtscher Ingo - We are reporting a rare case series of 2 siblings and their mother with diabetes having a gene mutation. - Source: PubMed
Publication date: 2024/08/19
Arshad KashanNaseem AamirHussain Syed SaddamMehak Noor-Ul-AinButt Awais MuhammadAftab SommayyaSaeed AnjumCheema Huma Arshad - Traumatic brain injury (TBI) due to a direct blow or penetrating injury to the head damages the brain tissue and affects brain function. Primary and secondary damage to the brain tissue increases disability, morbidity, and mortality and costs millions of dollars in treatment. Injury to the brain tissue results in the activation of various inflammatory and repair pathways involving many cellular and molecular factors. Increased infiltration of immune cells to clear the debris and lesion healing, activation of Schwann cells, myelination, oligodendrocyte formation, and axonal regeneration occur after TBI to regenerate the tissue. However, secondary damage to brain tissue results in behavioral symptoms. Repair and regeneration are regulated by a complex cascade involving various cells, hormones, and proteins. A change in the expression of various proteins due to altered gene expression may be the cause of impaired repair and the sequelae in TBI. In this pilot study, we used a Yucatan miniswine model of TBI with and without electromagnetic field (EMF) stimulation and investigated the differential gene expression between injured and non-injured cortex tissues. We found several differentially expressed genes including INSC, TTR, CFAP126, SEMA3F, CALB1, CDH19, and SERPINE1. These genes are associated with immune cell infiltration, myelination, reactive oxygen species regulation, thyroid hormone transportation, cell proliferation, and cell migration. There was a time-dependent effect of EMF stimulation on the gene and protein expression. The findings support the beneficial effect of EMF stimulation in the repair process following TBI. - Source: PubMed
Publication date: 2024/02/13
Rai VikrantMendoza-Mari YsselBrazdzionis JamesRadwan Mohamed MConnett David AMiulli Dan EAgrawal Devendra K - This study aims to comprehensively analyze the clinical characteristics and identify the differentially expressed genes associated with drug-resistant epilepsy (DRE) in patients with focal cortical dysplasia (FCD). - Source: PubMed
Publication date: 2024/03/16
Zhang KeYao HeYang JixueJia TianmingShan QiaoLi DongmingLi MengchunGan LingWang XinjunDong Yan - Germline mutations in genes encoding subunits of succinate dehydrogenase (SDH) are associated with hereditary paraganglioma and pheochromocytoma. Although most mutations in SDHB, SDHC and SDHD are intraexonic variants, large germline deletions may represent up to 10% of all variants but are rarely characterized at the DNA sequence level. Additional phenotypic effects resulting from deletions that affect neighboring genes are also not understood. We performed multiplex ligation-dependent probe amplification, followed by a simple long-range PCR 'chromosome walking' protocol to characterize breakpoints in 20 SDHx-linked paraganglioma-pheochromocytoma patients. Breakpoints were confirmed by conventional PCR and Sanger sequencing. Heterozygous germline deletions of up to 104 kb in size were identified in SDHB, SDHC, SDHD and flanking genes in 20 paraganglioma-pheochromocytoma patients. The exact breakpoint could be determined in 16 paraganglioma-pheochromocytoma patients of which 15 were novel deletions. In six patients proximal genes were also deleted, including PADI2, MFAP2, ATP13A2 (PARK9), CFAP126, TIMM8B and C11orf57. These genes were either partially or completely deleted, but did not modify the phenotype. This study increases the number of known SDHx deletions by over 50% and demonstrates that a significant proportion of large gene deletions can be resolved at the nucleotide level using a simple and rapid method. - Source: PubMed
Publication date: 2016/12/06
Hoekstra A Svan den Ende BJulià X Pvan Breemen LScheurwater KTops C MMalinoc ADevilee PNeumann H P HBayley J-P