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Search results for: TCF4

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#33983548   2021/05/13 To Up

The effect of Wnt/β-catenin pathway on the scleral remolding in the mouse during form deprivation.

Many reports have shown that Wnt/β-Catenin pathway is associated with a variety of diseases, but its role in the pathogenesis of myopia is still unknown. In order to clarify the role of Wnt/β-catenin pathway in the development of form deprivation myopia (FDM), this study investigated the expression of scleral Wls, β-catenin and TCF4 in mice model of form deprivation (FD) myopia.
Shuyu Hu, Sha Ouyang, Hanhan Liu, Daren Zhang, Zhihong Deng

1291 related Products with: The effect of Wnt/β-catenin pathway on the scleral remolding in the mouse during form deprivation.

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#33973063   2021/05/11 To Up

Causal influences of neuroticism on mental health and cardiovascular disease.

We investigated the relationship between neuroticism and 16 mental and 18 physical traits using summary results of genome-wide association studies for these traits. LD score regression was used to investigate genetic correlations between neuroticism and the 34 health outcomes. Mendelian randomization was performed to investigate mutual causal relationships between neuroticism and the 34 health outcomes. Neuroticism genetically correlates with a majority of health-related traits and confers causal effects on 12 mental traits (major depressive disorder (MDD), insomnia, subjective well-being (SWB, negatively), schizophrenia, attention-deficit/hyperactivity disorder, alcohol dependence, loneliness, anorexia nervosa, anxiety disorder, bipolar disorder, obsessive-compulsive disorder, and psychiatric disorders) and two physical diseases (cardiovascular disease and hypertensive disease). Conversely, MDD, SWB, and insomnia have a causal effect on neuroticism. We highlighted key genes contributing to the causal associations between neuroticism and MDD, including RBFOX1, RERE, SOX5, and TCF4, and those contributing to the causal associations between neuroticism and cardiovascular diseases, including MAD1L1, ARNTL, RERE, and SOX6. The present study indicates that genetic variation mediates the causal influences of neuroticism on mental health and cardiovascular diseases.
Fuquan Zhang, Ancha Baranova, Chao Zhou, Hongbao Cao, Jiu Chen, Xiangrong Zhang, Mingqing Xu

1865 related Products with: Causal influences of neuroticism on mental health and cardiovascular disease.

200 1000 tests10 ug100.00 ug1-99 mg/ml/ea price x 2100ug1 mg

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#33964297   2021/05/05 To Up

MYPT1, regulated by miR-19b-3p inhibits the progression of non-small cell lung cancer via inhibiting the activation of wnt/β-catenin signaling.

Myosin phosphatase targeting protein 1 (MYPT1) was identified to function as a tumor suppressor in several kinds of cancers, but its role and the molecular mechanisms in non-small cell lung cancer (NSCLC) remain undiscovered. Herein, we aimed to reveal MYPT1 expression pattern and role in NSCLC, and investigate the underlying mechanisms.
Yixin Wang, Lei Wang, Jia Guo, Siyao Zuo, Ziyu Wang, Shucheng Hua

1950 related Products with: MYPT1, regulated by miR-19b-3p inhibits the progression of non-small cell lung cancer via inhibiting the activation of wnt/β-catenin signaling.



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#33963287   2021/05/07 To Up

Transcription factor 4 controls positioning of cortical projection neurons through regulation of cell adhesion.

The establishment of neural circuits depends on precise neuronal positioning in the cortex, which occurs via a tightly coordinated process of neuronal differentiation, migration, and terminal localization. Deficits in this process have been implicated in several psychiatric disorders. Here, we show that the transcription factor Tcf4 controls neuronal positioning during brain development. Tcf4-deficient neurons become mispositioned in clusters when their migration to the cortical plate is complete. We reveal that Tcf4 regulates the expression of cell adhesion molecules to control neuronal positioning. Furthermore, through in vivo extracellular electrophysiology, we show that neuronal functions are disrupted after the loss of Tcf4. TCF4 mutations are strongly associated with schizophrenia and cause Pitt-Hopkins syndrome, which is characterized by severe intellectual disability. Thus, our results not only reveal the importance of neuronal positioning in brain development but also provide new insights into the potential mechanisms underlying neurological defects linked to TCF4 mutations.
Yandong Zhang, Zheping Cai, Guanglei Hu, Songhui Hu, Yafei Wang, Na Li, Saiyong Chen, Qiong Liu, Lanhui Zeng, Tianxiang Tang, Yilan Zhang, Lei Xiao, Yu Gu, Yunli Xie

1582 related Products with: Transcription factor 4 controls positioning of cortical projection neurons through regulation of cell adhesion.

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#33958710   2021/05/06 To Up

Comprehensive genetic analysis confers high diagnostic yield in 16 Japanese patients with corpus callosum anomalies.

Corpus callosum anomalies (CCA) is a common congenital brain anomaly with various etiologies. Although one of the most important etiologies is genetic factors, the genetic background of CCA is heterogenous and diverse types of variants are likely to be causative. In this study, we analyzed 16 Japanese patients with corpus callosum anomalies to delineate clinical features and the genetic background of CCAs. We observed the common phenotypes accompanied by CCAs: intellectual disability (100%), motor developmental delay (93.8%), seizures (60%), and facial dysmorphisms (50%). Brain magnetic resonance imaging showed colpocephaly (enlarged posterior horn of the lateral ventricles, 84.6%) and enlarged supracerebellar cistern (41.7%). Whole exome sequencing revealed genetic alterations in 9 of the 16 patients (56.3%), including 8 de novo alterations (2 copy number variants and variants in ARID1B, CDK8, HIVEP2, and TCF4) and a recessive variant of TBCK. De novo ARID1B variants were identified in three unrelated individuals, suggesting that ARID1B variants are major genetic causes of CCAs. A de novo TCF4 variant and somatic mosaic deletion at 18q21.31-qter encompassing TCF4 suggest an association of TCF4 abnormalities with CCAs. This study, which analyzes CCA patients usung whole exome sequencing, demonstrates that comprehensive genetic analysis would be useful for investigating various causal variants of CCAs.
Sachiko Miyamoto, Mitsuhiro Kato, Takuya Hiraide, Tadashi Shiohama, Tomohide Goto, Akira Hojo, Akio Ebata, Manabu Suzuki, Kozue Kobayashi, Pin Fee Chong, Ryutaro Kira, Hiroko Baber Matsushita, Hiroko Ikeda, Kyoko Hoshino, Mayumi Matsufuji, Nobuko Moriyama, Masayuki Furuyama, Tatsuya Yamamoto, Mitsuko Nakashima, Hirotomo Saitsu

2515 related Products with: Comprehensive genetic analysis confers high diagnostic yield in 16 Japanese patients with corpus callosum anomalies.

4 Arrays/Slide2 Pieces/Box4 Membranes/Box2 Pieces/Box4 Membranes/Box96 wells (1 kit)4 Arrays/Slide

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#33928346   2021/04/30 To Up

An oncolytic adenovirus delivering TSLC1 inhibits Wnt signaling pathway and tumor growth in SMMC-7721 xenograft mice model.

Tumor suppressor in lung cancer-1 (TSLC1) was first identified as a tumor suppressor for lung cancer, and frequently downregulated in various types of cancers including hepatocellular carcinoma (HCC). The Wnt pathway plays a critical role in tumorigenesis, migration, and invasion in HCC. However, the function of TSLC1 in modulating Wnt signaling in HCC is unclear. In this study, we evaluated the effect of TSLC1-armed oncolytic adenovirus (S24-TSLC1) on the Wnt/β-catenin pathway, cell viability, invasion and migration abilities of HCC in vitro and the growth of SMMC-7721-xenografted tumor in mice model. We detected the expression of TSLC1 in tumor samples and HCC cell lines. The results showed that TSLC1 expression was low in HCC, but high in pericarcinomatous tissue and normal cells, which implied that TSLC1 is a tumor suppressor of liver cancer. S24-TSLC1 exhibited an antitumor effect on HCC cell growth in vitro, but did little damage to normal liver cells. Overexpression of TSLC1 downregulated the transcriptional activity of TCF4/β-catenin and inhibited the mRNA or protein expression of Wnt target genes cyclinD1 and c-myc. S24-TSLC1 also inhibited the invasion and migration of HCC cells. Animal experiments further confirmed that S24-TSLC1 significantly inhibited tumor growth of the SMMC-7721-xenografted tumor. In conclusion, TSLC1 could downregulate the Wnt signal pathway and suppress HCC cell growth, migration and invasion, suggesting that S24-TSLC1 may be a potent antitumor agent for future clinical trials in liver cancer treatment.
Yigang Wang, Panpan Huang, Yanping Hu, Keni Guo, Xiaoyuan Jia, Biao Huang, Xinyuan Liu, Xianglei He, Fang Huang

1718 related Products with: An oncolytic adenovirus delivering TSLC1 inhibits Wnt signaling pathway and tumor growth in SMMC-7721 xenograft mice model.

2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box

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#33917757   2021/04/08 To Up

PGC1α Loss Promotes Lung Cancer Metastasis through Epithelial-Mesenchymal Transition.

PGC1α oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. Transcriptome and in vivo xenograft analysis show that a decreased PGC1α correlates with the epithelial-mesenchymal transition (EMT) and lung cancer metastasis. The deletion of a single Pgc1α allele in mice promotes bone metastasis of Kras-driven lung cancer. Mechanistically, PGC1α predominantly activates ID1 expression, which interferes with TCF4-TWIST1 cooperation during EMT. Bioinformatic and clinical studies have shown that PGC1α and ID1 are downregulated in lung cancer, and correlate with a poor survival rate. Our study indicates that TCF4-TWIST1-mediated EMT, which is regulated by the PGC1α-ID1 transcriptional axis, is a potential diagnostic and therapeutic target for metastatic lung cancer.
Taek-In Oh, Mingyu Lee, Yoon-Mi Lee, Geon-Hee Kim, Daekee Lee, Jueng Soo You, Sun Ha Kim, Minyoung Choi, Hyonchol Jang, Yeong-Min Park, Hyun-Woo Shin, Dong Hoon Shin, Ji-Hong Lim

1168 related Products with: PGC1α Loss Promotes Lung Cancer Metastasis through Epithelial-Mesenchymal Transition.

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#33871149   2021/04/19 To Up

CDK14/β-catenin/TCF4/miR-26b positive feedback regulation modulating pancreatic cancer cell phenotypes in vitro and tumor growth in mice model in vivo.

Chemotherapy and radiotherapy have been reported to be basically ineffective for pancreatic ductal adenocarcinoma (PDAC) patients; thus, gene therapy might provide a novel approach for them. CDK14, a new oncogenic member of CDK family involving in pancreatic cancer cell response to Gemcitabine (GEM) treatment, has been reported to be regulated by miRNAs. In this study, we aimed to investigate whether miR-26b regulated CDK14 expression to affect the phenotype of pancreatic cancer cells.
Yunpeng Sun, Pengfei Wang, Qiyu Zhang, Huanhuan Wu

1026 related Products with: CDK14/β-catenin/TCF4/miR-26b positive feedback regulation modulating pancreatic cancer cell phenotypes in vitro and tumor growth in mice model in vivo.

96 wells

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