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Kunliang guan

Beiyun Zhou, Per Flodby, Jiao Luo, Dan R Castillo, Yixin Liu, Fa-Xing Yu, Alicia McConnell, Bino Varghese, Guanglei Li, Nyam-Osor Chimge, Mitsuhiro Sunohara, Michael N Koss, Wafaa Elatre, Peter Conti, Janice M Liebler, Chenchen Yang, Crystal N Marconett, Ite A Laird-Offringa, Parviz Minoo, Kunliang Guan, Barry R Stripp, Edward D Crandall, Zea Borok
Claudins, the integral tight junction (TJ) proteins that regulate paracellular permeability and cell polarity, are frequently dysregulated in cancer; however, their role in neoplastic progression is unclear. Here, we demonstrated that knockout of Cldn18, a claudin family member highly expressed in lung alveolar epithelium, leads to lung enlargement, parenchymal expansion, increased abundance and proliferation of known distal lung progenitors, the alveolar epithelial type II (AT2) cells, activation of Yes-associated protein (YAP), increased organ size, and tumorigenesis in mice...
March 1, 2018: Journal of Clinical Investigation
Yijun Gao, Wenjing Zhang, Xiangkun Han, Fuming Li, Xujun Wang, Rui Wang, Zhaoyuan Fang, Xinyuan Tong, Shun Yao, Fei Li, Yan Feng, Yihua Sun, Yingyong Hou, Zhongzhou Yang, Kunliang Guan, Haiquan Chen, Lei Zhang, Hongbin Ji
Whether the Hippo pathway contributes to cell lineage transition under pathological conditions, especially tumorigenesis, remains largely unknown. Here we show that YAP, the major effector of the Hippo pathway, displays a distinct activation pattern in lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC); YAP is initially activated by LKB1 loss in lung ADC, which upregulates ZEB2 expression and represses DNp63 transcription in a default manner. During transdifferentiation, YAP is inactivated, which in turn relieves ZEB2-mediated default repression of DNp63 and triggers squamous differentiation reprogramming...
August 13, 2014: Nature Communications
Hui Yang, Huaipeng Lin, Haiyan Xu, Lei Zhang, Lu Cheng, Bo Wen, Jianyong Shou, Kunliang Guan, Yue Xiong, Dan Ye
No abstract text is available yet for this article.
August 2014: Cell Research
Hui Yang, Yue Xiong, KunLiang Guan
Altered metabolism in cancer was first discovered by Otto Warburg early last century. Although the Warburg Effect has been widely used in tumor detection, relatively little progress had been made in mechanistic understanding of cancer metabolism in the subsequent eight decades. Genetic studies have recently identified mutations in human cancer targeting multiple enzymes involved in intermediate metabolism. One emerging mechanism common to these mutant enzymes is the accumulation of a metabolite that alters the epigenetic control...
December 2013: Science China. Life Sciences
Jia Chang, Zhuo Wang, Eric Tang, Zhipeng Fan, Laurie McCauley, Renny Franceschi, Kunliang Guan, Paul H Krebsbach, Cun-Yu Wang
An imbalance in bone formation relative to bone resorption results in the net bone loss that occurs in osteoporosis and inflammatory bone diseases. Although it is well known how bone resorption is stimulated, the molecular mechanisms that mediate impaired bone formation are poorly understood. Here we show that the time- and stage-specific inhibition of endogenous inhibitor of kappaB kinase (IKK)--nuclear factor-kappaB (NF-kappaB) in differentiated osteoblasts substantially increases trabecular bone mass and bone mineral density without affecting osteoclast activities in young mice...
June 2009: Nature Medicine
Yadong Yu, Sheng Li, Xiang Xu, Yong Li, Kunliang Guan, Eddy Arnold, Jianping Ding
The small GTPase Rheb displays unique biological and biochemical properties different from other small GTPases and functions as an important mediator between the tumor suppressor proteins TSC1 and TSC2 and the mammalian target of rapamycin to stimulate cell growth. We report here the three-dimensional structures of human Rheb in complexes with GDP, GTP, and GppNHp (5'-(beta,gamma-imide)triphosphate), which reveal novel structural features of Rheb and provide a molecular basis for its distinct properties. During GTP/GDP cycling, switch I of Rheb undergoes conformational change while switch II maintains a stable, unusually extended conformation, which is substantially different from the alpha-helical conformation seen in other small GTPases...
April 29, 2005: Journal of Biological Chemistry
Min Wang, Theodora R Devereux, Haris G Vikis, Scott D McCulloch, Wanda Holliday, Colleen Anna, Yian Wang, Katarzyna Bebenek, Thomas A Kunkel, Kunliang Guan, Ming You
In this study, we performed systematic candidate gene analyses of the Pulmonary adenoma resistance 2 locus. Differential gene expression in lung tissues and nucleotide polymorphisms in coding regions between A/J and BALB/cJ mice were examined using reverse transcription-PCR and direct sequencing. Although not all genes in the interval were analyzed at this moment due to the recent database updating, we have found that the Pol iota gene, encoding the DNA polymerase iota, contains 25 nucleotide polymorphisms in its coding region between A/J and BALB/cJ mice, resulting in a total of ten amino acid changes...
March 15, 2004: Cancer Research
Suqing Xie, Qi Wang, Qin Ruan, Tongyi Liu, Meena Jhanwar-Uniyal, Kunliang Guan, Wei Dai
MEK1, a gene product that regulates cell growth and differentiation, also plays an important role in Golgi breakdown during the cell cycle. We have recently shown that polo-like kinase (Plk3) is Golgi localized and involved in Golgi dynamics during the cell cycle. To study the mode of action of Plk3 in the Golgi fragmentation cascade, we examined functional as well as physical interactions between Plk3 and MEK1/ERKs. In HeLa cells, although a significant amount of Plk3 signals dispersed in a manner similar to those of Golgi during mitosis concentrated Plk3 was detected at spindle poles, which colocalized with phospho-MEKs and phospho-ERKs...
May 6, 2004: Oncogene
Qin Ruan, Qi Wang, Suqing Xie, Yuqiang Fang, Zbigniew Darzynkiewicz, Kunliang Guan, Meena Jhanwar-Uniyal, Wei Dai
The Golgi apparatus undergoes extensive fragmentation during mitosis in animal cells. Protein kinases play a critical role during fragmentation of the Golgi apparatus. We reported here that Polo-like kinase 3 (Plk3) may be an important mediator during Golgi breakdown. Specifically, Plk3 was concentrated at the Golgi apparatus in HeLa and A549 cells during interphase. At the onset of mitosis, Plk3 signals disintegrated and redistributed in a manner similar to those of Golgi stacks. Nocodazole activated Plk3 kinase activity, correlating with redistribution of Plk3 signals and Golgi fragmentation...
March 10, 2004: Experimental Cell Research
Fan Yang, Junro Yamashita, Eric Tang, Hom-Lay Wang, Kunliang Guan, Cun-Yu Wang
The activation of the I-kappaB kinase (IKK) complex by TNF or LPS stimulates phosphorylation and degradation of I-kappaBalpha, leading to the nuclear translocation of NF-kappaB. The IKK complex is mainly composed of two catalytic subunits, IKKalpha and IKKbeta, and a chaperon subunit IKKgamma. Although IKKgamma does not have catalytic activity, it is essential for IKK activation induced by multiple stimuli. Importantly, the key residue cysteine 417 at the zinc finger domain of IKKgamma has been found to be mutated to arginine (IKKgammaC417R) in a human genetic disorder called the anhydrotic ectodermal dysplasia with immunodeficiency...
February 15, 2004: Journal of Immunology: Official Journal of the American Association of Immunologists
Qunmin Zhou, Kottil Rammohan, Shili Lin, Nikki Robinson, Ou Li, Xingluo Liu, Xue-feng Bai, Lijie Yin, Bruce Scarberry, Peishuang Du, Ming You, Kunliang Guan, Pan Zheng, Yang Liu
Multiple sclerosis (MS) is a chronic neurological disease of unknown etiology, but a genetic basis for the disease is undisputed. We have reported that CD24 is required for the pathogenicity of autoreactive T cells in experimental autoimmune encephalomyelitis, the mouse model of MS. Here we investigate the contribution of CD24 to MS by studying single-nucleotide polymorphism in the ORF among 242 MS patients and 207 population controls. This single-nucleotide polymorphism results in replacement of alanine (CD24a) with valine (CD24v) in the mature protein...
December 9, 2003: Proceedings of the National Academy of Sciences of the United States of America
Joyce H Hurley, Shengwen Zhang, Leighan S Bye, Mark S Marshall, Anna A DePaoli-Roach, Kunliang Guan, Aaron P Fox, Lei Yu
BACKGROUND: G protein-coupled receptors (GPCRs) interact with heterotrimeric GTP-binding proteins (G proteins) to modulate acute changes in intracellular messenger levels and ion channel activity. In contrast, long-term changes in cellular growth, proliferation and differentiation are often mediated by tyrosine kinase receptors and certain GPCRs by activation of mitogen-activated protein (MAP) kinases. Complex interactions occur between these signaling pathways, but the specific mechanisms of such regulatory events are not well-understood...
June 9, 2003: BMC Neuroscience
Fan Yang, Eric Tang, Kunliang Guan, Cun-Yu Wang
Activation of the I kappa B kinase (IKK) complex by LPS induces phosphorylation and degradation of I kappa B alpha, leading to the nuclear translocation of NF-kappa B. Although it is essential for NF-kappa B activation, emerging evidence has indicated that the nuclear translocation of NF-kappa B is not sufficient to activate NF-kappa B-dependent transcription. Here, we reported that LPS induced the phosphorylation of the p65 trans-activation domain on serine 536 in monocytes/macrophages. Using mouse embryonic fibroblasts lacking either IKK alpha or IKK beta, we found that IKK beta played an essential role in LPS-induced p65 phosphorylation on serine 536, while IKK alpha was partially required for the p65 phosphorylation...
June 1, 2003: Journal of Immunology: Official Journal of the American Association of Immunologists
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