Identification, Characterization, and Effects of<i>Xenopus laevis</i>PNAS-4 Gene on Embryonic Development

Yan, Fei; Ruan, Xiuhang; Yang, Huiling; Yao, Su; Zhao, Xinyu; Gou, Lantu; Ma, Fei; Zhu, Yong‐Guan; Deng, Hongxin; Wei, Yuquan

doi:10.1155/2010/134764

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…A previous study demonstrated that the overexpression and depletion of DESI-2 in embryos was able to induce developmental defects in Xenopus and zebrafish animal models, indicating that DESI-2 is crucial for the maintenance of basic cellular activities (9,10). In our previous study, it was demonstrated that DESI-2 is located at the Golgi apparatus in the cytoplasm and that its expression levels are decreased in pancreatic cancer tissues (4).…”

Section: Introductionmentioning

confidence: 85%

Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells

Kang

Shen

et al. 2016

Oncology Letters

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Abstract. Human desumoylating isopeptidase 2 (DESI-2) is a member of the DESI family and contains a conserved PPPDE1 domain. Previous studies have demonstrated that DESI-2 overexpression may induce cell apoptosis. In the present study, differentially expressed genes were analyzed using a transcription microarray in DESI-2 overexpressing PANC-1 pancreatic cancer cells. A total of 45,033 genes were examined by microarray, which identified 1,766 upregulated and 1,643 downregulated genes. A series of altered signaling pathways were analyzed, in which certain essential signaling factors, including retinoid X receptor (RXR), BH3 interacting-domain death agonist, Ras homolog gene family member A (RhoA) and Rho-associated protein kinase, were further investigated at the protein level. The release of cytochrome c and the activation of caspase-3 were also detected by western blot analysis. Immunohistochemistry further revealed the expression features of RXR and RhoA in pancreatic ductal adenocarcinoma tissues with various DESI-2 expression levels. The results serve as a valuable reference for the further elucidation of the functions of DESI-2 in pancreatic cancer.

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Section: Introductionmentioning

confidence: 85%

Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells

Kang

Shen

et al. 2016

Oncology Letters

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“… 251 This phenotype is rescued by blocking the miR-199 binding site, demonstrating a distinct role of miRNAs in eye development and ocular maldevelopment, and a novel set of targets for drug treatments. Additional candidates for patient screens originating from Xenopus overexpression modelling include siah-2 , 252 , 253 E - NTPDase , 254 PNAS-4 255 and pparγ 256 and knockdowns of sdr16c5 , 257 frs3 258 and psf2. 259 Although none of the candidates listed have yet been identified in microphthalmic cohorts, as frequency of next-generation sequencing escalates and large databases such as from the 100,000 genomes project can be analysed in more depth, there is increased capability to identify novel genes in patients through screening performed in animal models.…”

Section: Animal Models Of Microphthalmiamentioning

confidence: 99%

Animal and cellular models of microphthalmia

Harding¹,

Cunha²,

Moosajee

2021

Therapeutic Advances in Rare Disease

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Microphthalmia is a rare developmental eye disorder affecting 1 in 7000 births. It is defined as a small (axial length ⩾2 standard deviations below the age-adjusted mean) underdeveloped eye, caused by disruption of ocular development through genetic or environmental factors in the first trimester of pregnancy. Clinical phenotypic heterogeneity exists amongst patients with varying levels of severity, and associated ocular and systemic features. Up to 11% of blind children are reported to have microphthalmia, yet currently no treatments are available. By identifying the aetiology of microphthalmia and understanding how the mechanisms of eye development are disrupted, we can gain a better understanding of the pathogenesis. Animal models, mainly mouse, zebrafish and Xenopus, have provided extensive information on the genetic regulation of oculogenesis, and how perturbation of these pathways leads to microphthalmia. However, differences exist between species, hence cellular models, such as patient-derived induced pluripotent stem cell (iPSC) optic vesicles, are now being used to provide greater insights into the human disease process. Progress in 3D cellular modelling techniques has enhanced the ability of researchers to study interactions of different cell types during eye development. Through improved molecular knowledge of microphthalmia, preventative or postnatal therapies may be developed, together with establishing genotype–phenotype correlations in order to provide patients with the appropriate prognosis, multidisciplinary care and informed genetic counselling. This review summarises some key discoveries from animal and cellular models of microphthalmia and discusses how innovative new models can be used to further our understanding in the future. Plain language summary Animal and Cellular Models of the Eye Disorder, Microphthalmia (Small Eye) Microphthalmia, meaning a small, underdeveloped eye, is a rare disorder that children are born with. Genetic changes or variations in the environment during the first 3 months of pregnancy can disrupt early development of the eye, resulting in microphthalmia. Up to 11% of blind children have microphthalmia, yet currently no treatments are available. By understanding the genes necessary for eye development, we can determine how disruption by genetic changes or environmental factors can cause this condition. This helps us understand why microphthalmia occurs, and ensure patients are provided with the appropriate clinical care and genetic counselling advice. Additionally, by understanding the causes of microphthalmia, researchers can develop treatments to prevent or reduce the severity of this condition. Animal models, particularly mice, zebrafish and frogs, which can also develop small eyes due to the same genetic/environmental changes, have helped us understand the genes which are important for eye development and can cause birth eye defects when disrupted. Studying a patient’s own cells grown in the laboratory can further help researchers understand how changes in genes affect their function. Both animal and cellular models can be used to develop and test new drugs, which could provide treatment options for patients living with microphthalmia. This review summarises the key discoveries from animal and cellular models of microphthalmia and discusses how innovative new models can be used to further our understanding in the future.

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“…Our previous study showed that overexpression of PPPDE1 could induce apoptosis of human lung adenocarcinoma A549 cells ( 4 ). In addition, mRNA microinjection of PPPDE1 in zebrafish and Xenopus embryos resulted in developmental defects, indicating essential roles of PPPDE1 in embryonic development ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Implications of PPPDE1 expression in the distribution of plakoglobin and β-catenin in pancreatic ductal adenocarcinoma

et al. 2014

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Human PPPDE peptidase domain-containing protein 1 (PPPDE1) is a recently identified protein; however, its exact functions remain unclear. In our previous study, the PPPDE1 protein was found to be decreased in certain cancer tissues. In the present study, a total of 96 pancreatic ductal carcinoma tissue samples and 31 normal tissues samples were assessed to investigate the distribution of plakoglobin and β-catenin under the conditions of various PPPDE1 expression levels by means of immunohistochemistry. Generally, the staining of PPPDE1 was strong in normal tissues, but weak in cancer tissues. Plakoglobin was mainly distributed along the membrane and cytoplasm border in normal cells, but was less evident in the membranes of cancer cells. In particular, a greater percentage of cells exhibited low membrane plakoglobin expression in cancer tissue with low PPPDE1 expression (PPPDE1-low cancer) compared with that in cancer tissue with high PPPDE1 expression (PPPDE1-high cancer). The distribution of β-catenin in normal tissues was similar to that of plakoglobin. However, β-catenin was peculiarly prone to invade nucleus in PPPDE1-low cancer compared with PPPDE1-high cancer. Our data suggested potential links between PPPDE1 expression and the distribution of plakoglobin and β-catenin in pancreatic ductal adenocarcinoma, providing insights into the role of PPPDE1 in the progression of pancreatic cancer.

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Identification, Characterization, and Effects ofXenopus laevisPNAS-4 Gene on Embryonic Development

Cited by 6 publications

References 28 publications

Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells

Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells

Animal and cellular models of microphthalmia

Implications of PPPDE1 expression in the distribution of plakoglobin and β-catenin in pancreatic ductal adenocarcinoma

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