Yi‐Chao Lee

Taipei Medical University

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Chi-Chen Huang

Taipei Medical University

Yen‐Nien Liu

Taipei Medical University

Jiaoti Huang

Duke University

Shaoxi Niu

Chinese PLA General Hospital

Huaiyin Shi

Chinese PLA General Hospital

Jinhang Li

Southwest University

Yulei Tao

University of Oklahoma Health Sciences Center

Kuen‐Haur Lee

Taipei Medical University

Qingfu Zhang

China Medical University

Kuo‐Ching Jiang

Taipei Medical University

Cooperative Institutions

Institute of Molecular Biology and Biophysics

256

National Cheng Kung University

154

Taipei Medical University

131

National Yang Ming Chiao Tung University

Academia Sinica

Kaohsiung Medical University

National Taiwan University

National Health Research Institutes

Institute of Biomedical Sciences, Academia Sinica

National Defense Medical Center

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Figure S5 from Leukemia Inhibitory Factor Promotes Castration-resistant Prostate Cancer and Neuroendocrine Differentiation by Activated ZBTB46

Yen‐Nien Liu Shaoxi Niu Weiyu Chen Qingfu Zhang Yulei Tao

<p>Supplementary Figure S5</p>

Factor (programming language)

Neuroendocrine differentiation

10.1158/1078-0432.22470719.v1

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Figure S5 from Leukemia Inhibitory Factor Promotes Castration-resistant Prostate Cancer and Neuroendocrine Differentiation by Activated ZBTB46

Yen‐Nien Liu Shaoxi Niu Weiyu Chen Qingfu Zhang Yulei Tao

<p>Supplementary Figure S5</p>

Neuroendocrine differentiation

Factor (programming language)

10.1158/1078-0432.22470719

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Increase of Zinc Finger Protein 179 in Response to CCAAT/Enhancer Binding Protein Delta Conferring an Antiapoptotic Effect in Astrocytes of Alzheimer’s Disease

Molecular Neurobiology (2014)

Shao-Ming Wang Yi‐Chao Lee Chiung Yuan Ko Ming Derg Lai Ding-Yen Lin

Reactive astrogliosis is a cellular manifestation of neuroinflammation and occurs in response to all forms and severities of the central nervous system (CNS)'s injury and disease. Both astroglial proliferation and antiapoptotic processes are aspects of astrogliosis. However, the underlying mechanism of this response remains poorly understood. In addition, little is known about why activated astrocytes are more resistant to stress and inflammation. CCAAT/enhancer binding protein delta (CEBPD) is a transcription factor found in activated astrocytes that surround β-amyloid plaques. In this study, we found that astrocytes activation was attenuated in the cortex and hippocampus of APPswe/PS1 E9 (AppTg)/Cebpd (-/-)mice. Furthermore, an increase in apoptotic astrocytes was observed in AppTg/Cebpd (-/-)mice, suggesting that CEBPD plays a functional role in enhancing the antiapoptotic ability of astrocytes. We found that Zinc Finger Protein 179 (ZNF179) was a CEBPD-regulated gene that played an antiapoptotic, but not proliferative, role in astrocytes. The transcriptions of the proapoptotic genes, insulin-like growth factor binding protein 3 (IGFBP3) and BCL2-interacting killer (BIK), were suppressed by ZNF179 via its interaction with the promyelocytic leukemia zinc finger (PLZF) protein in astrocytes. This study provides the first evidence that ZNF179, PLZF, IGFBP3, and BIK contributed to the novel CEBPD-induced antiapoptotic feature of astrocytes.

Astrogliosis

Ccaat-enhancer-binding proteins

10.1007/s12035-014-8714-9

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Comparison of EPS Extraction Efficiences from Spirogyra fluviatilis by Chemical and Physical Extraction Methods

International Journal of Bioscience Biochemistry and Bioinformatics (2019)

Shui‐Ping Chang Hwey‐Lin Sheu Yi‐Chao Lee

Spirogyra

10.17706/ijbbb.2019.9.4.202-209

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Citations (7)

Glucocorticoid upregulates Na-K-ATPase alpha- and beta-mRNA via an indirect mechanism in proximal tubule cell primary cultures

AJP Renal Physiology (1995)

Yi‐Chao Lee Hsi‐Hui Lin Ming‐Jer Tang

Adrenalectomy leads to the decline in the levels of renal Na-K-adenosinetriphosphatase (Na-K-ATPase) alpha- and beta-subunit protein and mRNA. Both alpha- and beta-mRNA, however, return to the control level within 1 h after corticosterone administration. Whether or not glucocorticoid acts directly on a specific segment of nephron to upregulate Na-K-ATPase has not been determined. Studies were undertaken in an attempt to elucidate this problem. Using primary cultures of renal proximal tubules, we found that 24-h treatment with dexamethasone augmented Na-K-ATPase activity and induced coordinate increase of alpha- and beta-protein and mRNA abundance dependent on the doses in the range of 10(-8) to 10(-6) M. We further demonstrated that 24-h incubation of dexamethasone (10(-7) M) enhanced Na-K-ATPase activity by 58 +/- 14%, alpha- and beta-protein abundance by 70 +/- 18 and 51 +/- 10%, and alpha- and beta-mRNA levels by 87 +/- 12 and 62 +/- 11%, respectively. The time course studies revealed that significant increase of Na-K-ATPase activity and alpha and beta-protein abundance was reached within 4 hr of dexamethasone treatment. Pretreatment of cultured proximal tubule cells with cycloheximide (20 micrograms/ml) completely inhibited dexamethasone-induced increase of Na-K-ATPase alpha- and beta-mRNA. Our results indicate that dexamethasone upregulates Na-K-ATPase in proximal tubule cells via pretranslational mechanisms, which may be mediated by proteins.

Alpha (finance)

BETA (programming language)

10.1152/ajprenal.1995.268.5.f862

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A novel RING finger protein, Znf179, modulates cell cycle exit and neuronal differentiation of P19 embryonal carcinoma cells

Cell Death and Differentiation (2011)

P-C Pao N-K Huang Y-W Liu S-H Yeh Lin St

Znf179 is a member of the RING finger protein family. During embryogenesis, Znf179 is expressed in a restricted manner in the brain, suggesting a potential role in nervous system development. In this report, we show that the expression of Znf179 is upregulated during P19 cell neuronal differentiation. Inhibition of Znf179 expression by RNA interference significantly attenuated neuronal differentiation of P19 cells and a primary culture of cerebellar granule cells. Using a microarray approach and subsequent functional annotation analysis, we identified differentially expressed genes in Znf179-knockdown cells and found that several genes are involved in development, cellular growth, and cell cycle control. Flow cytometric analyses revealed that the population of G0/G1 cells decreased in Znf179-knockdown cells. In agreement with the flow cytometric data, the number of BrdU-incorporated cells significantly increased in Znf179-knockdown cells. Moreover, in Znf179-knockdown cells, p35, a neuronal-specific Cdk5 activator that is known to activate Cdk5 and may affect the cell cycle, and p27, a cell cycle inhibitor, also decreased. Collectively, these results show that induction of the Znf179 gene may be associated with p35 expression and p27 protein accumulation, which lead to cell cycle arrest in the G0/G1 phase, and is critical for neuronal differentiation of P19 cells.

P19 cell

10.1038/cdd.2011.52

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Citations (31)

RINT-1 interacts with MSP58 within nucleoli and plays a role in ribosomal gene transcription

Biochemical and Biophysical Research Communications (2016)

Chuan-Pin Yang Yu-Liang Kuo Yi‐Chao Lee Kuen‐Haur Lee Chi-Wu Chiang

ribosome biogenesis

Transcription

RNA polymerase I

Chromatin immunoprecipitation

Ribosomal protein

10.1016/j.bbrc.2016.08.044

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Journal of Biological Chemistry (2014)

Jae Min Lee Umut Özcan Rachel Liberman Sarah Bond Mara G. Shainheit

On The CoverConfocal microscopy image of a ventricular myocyte from an adult rat heart, with nuclei stained with DAPI (blue) and cardiac myosin-binding protein C (green) and telethonin (red) immunolabeled with specific antibodies.Telethonin is localized to the Z-disc regions of cardiac sarcomeres, where its function may be regulated by phosphorylation of two Ser residues in the C-terminal region of the protein.For details see the article by Candasamy et al., pages

10.1016/s0021-9258(20)33659-0

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Modular patterning of structure and function of the striatum by retinoid receptor signaling

Proceedings of the National Academy of Sciences (2008)

Wenlin Liao Hsiu‐Chao Tsai Hsiao‐Fang Wang Josephine Chang Kuan-Ming Lu

Retinoid signaling plays a crucial role in patterning rhombomeres in the hindbrain and motor neurons in the spinal cord during development. A fundamentally interesting question is whether retinoids can pattern functional organization in the forebrain that generates a high order of cognitive behavior. The striatum contains a compartmental structure of striosome (or “patch”) and intervening matrix. How this highly complex mosaic design is patterned by the genetic programs during development remains elusive. We report a developmental mechanism by which retinoid receptor signaling controls compartmental formation in the striatum. We analyzed RARβ −/− mutant mice and found a selective loss of striosomal compartmentalization in the rostral mutant striatum. The loss of RARβ signaling in the mutant mice resulted in reduction of cyclin E2, a cell cycle protein regulating transition from G 1 to S phase, and also reduction of the proneural gene Mash1 , which led to defective neurogenesis of late-born striosomal cells. Importantly, during striatal neurogenesis, endogenous levels of retinoic acid were spatiotemporally regulated such that transduction of high levels of retinoic acid through RARβ selectively expanded the population of late-born striosomal progenitors, which evolved into a highly elaborate compartment in the rostral striatum. RARβ −/− mutant mice, which lacked such enlarged compartment, displayed complex alternations of dopamine agonist-induced stereotypic motor behavior, including exaggeration of head bobbing movement and reduction of rearing activity. RARβ signaling thus plays a crucial role in setting up striatal compartments that may engage in neural circuits of psychomotor control.

Forebrain

Hindbrain

10.1073/pnas.0802109105

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Citations (69)

When Cytokinin, a Plant Hormone, Meets the Adenosine A2A Receptor: A Novel Neuroprotectant and Lead for Treating Neurodegenerative Disorders?

PLoS ONE (2012)

Yi‐Chao Lee Ying-Chen Yang Chuen-Lin Huang Tsun-Yung Kuo Jung‐Hsin Lin

It is well known that cytokinins are a class of phytohormones that promote cell division in plant roots and shoots. However, their targets, biological functions, and implications in mammalian systems have rarely been examined. In this study, we show that one cytokinin, zeatin riboside, can prevent pheochromocytoma (PC12) cells from serum deprivation-induced apoptosis by acting on the adenosine A2A receptor (A2A-R), which was blocked by an A2A-R antagonist and a protein kinase A (PKA) inhibitor, demonstrating the functional ability of zeatin riboside by mediating through A2A-R signaling event. Since the A2A-R was implicated as a therapeutic target in treating Huntington's disease (HD), a cellular model of HD was applied by transfecting mutant huntingtin in PC12 cells. By using filter retardation assay and confocal microscopy we found that zeatin riboside reversed mutant huntingtin (Htt)-induced protein aggregations and proteasome deactivation through A2A-R signaling. PKA inhibitor blocked zeatin riboside-induced suppression of mutant Htt aggregations. In addition, PKA activated proteasome activity and reduced mutant Htt protein aggregations. However, a proteasome inhibitor blocked both zeatin riboside-and PKA activator-mediated suppression of mutant Htt aggregations, confirming mediation of the A2A-R/PKA/proteasome pathway. Taken together, zeatin riboside might have therapeutic potential as a novel neuroprotectant and a lead for treating neurodegenerative disorders.

Riboside

Adenosine A2A receptor

10.1371/journal.pone.0038865

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Citations (27)