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Journal articles on the topic 'PlxnA1'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Zhang, Xiaoli, Shuai Shao, and Lang Li. "Characterization of Class-3 Semaphorin Receptors, Neuropilins and Plexins, as Therapeutic Targets in a Pan-Cancer Study." Cancers 12, no. 7 (2020): 1816. http://dx.doi.org/10.3390/cancers12071816.

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Class-3 semaphorins (SEMA3s), initially characterized as axon guidance cues, have been recognized as key regulators for immune responses, angiogenesis, tumorigenesis and drug responses. The functions of SEMA3s are attributed to the activation of downstream signaling cascades mainly mediated by cell surface receptors neuropilins (NRPs) and plexins (PLXNs), yet their roles in human cancers are not completely understood. Here, we provided a detailed pan-cancer analysis of NRPs and PLXNs in their expression, and association with key signal transducers, patient survival, tumor microenvironment (TME

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Kuroiwa, A., F. Suto, H. Fujisawa, and Y. Matsuda. "Chromosome assignment of four plexin A genes (Plxna1, Plxna2, Plxna3, Plxna4) in mouse, rat, Syrian hamster and Chinese hamster." Cytogenetic and Genome Research 92, no. 1-2 (2001): 127–29. http://dx.doi.org/10.1159/000056882.

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3

Miyamoto, Yuji, Fotios Loupakis, Wu Zhang, et al. "Genetic variations in semaphorin/neuropilin signaling to predict clinical outcome in patients (pts) with metastatic colorectal cancer (mCRC) receiving bevacizumab-based chemotherapy." Journal of Clinical Oncology 35, no. 15_suppl (2017): 11608. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.11608.

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11608 Background: Neuropilin ( NRP) is known to be an important VEGF co-receptor that acts as a key mediator of angiogenesis. Its ligands, semaphorins ( SEMA), compete with VEGF for NRP binding and can themselves have angiogenic activity. Plexins are also receptors of SEMAs, and have the GTPase activating proteins (GAPs) domain for RAS. NRPs are shown to signal through RAS pathways. We aimed to evaluate whether single nucleotide polymorphisms (SNPs) of genes involved in the SEMA/NRPpathways predict clinical outcome in bevacizumab-treated mCRC pts. Methods: Associations between nine SNPs in 7 g

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Park, Sangwook, Ji-Eun Oh, and Hyun-Seok Jin. "Recapitulation of the Genetic Association of PLXNA2 with Bone Density and Osteoporosis via In Vitro Experiments Using a Korean Female Cohort." Journal of Medical Imaging and Health Informatics 10, no. 6 (2020): 1418–22. http://dx.doi.org/10.1166/jmihi.2020.3064.

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Osteoporosis is a bone disorder in which the imbalance of osteoclasts and osteoblasts leads to bone-destructive diseases especially among elderly women. Several factors, including genetic and environmental factors, contribute to the pathogenesis of these diseases. Bone mineral density (BMD) is a robust factor that influences osteoporosis; the development of osteoporosis in the elderly is estimated based on the BMD. Our previous microarray assay using murine preosteoblast cells revealed that Plexin A2 is associated with the differentiation and mineralization of bone-forming osteoblasts via bone

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Oleari, Roberto, Alessia Caramello, Sara Campinoti, et al. "PLXNA1 and PLXNA3 cooperate to pattern the nasal axons that guide gonadotropin-releasing hormone neurons." Development 146, no. 21 (2019): dev176461. http://dx.doi.org/10.1242/dev.176461.

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6

Dormon, Katherine, Elda S. Latif, Matthew Bashton, et al. "A Whole Genome In Vivo Crispr Screen in Primary ALL Predicts Leukaemic Relapse." Blood 126, no. 23 (2015): 2619. http://dx.doi.org/10.1182/blood.v126.23.2619.2619.

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Abstract Although paediatric acute lymphoblastic leukaemia (ALL) has a favourable prognosis, a number of cases will invariably relapse. One of the major problems associated with relapse is drug resistance, in particular to glucocorticoids, the mainstay of ALL treatment. Examining the underlying mechanisms is complicated by clonal heterogeneity within a patient and the potential impact of the leukaemic niche. To address mechanisms of drug resistance in a patient-relevant setting, we performed a genome-wide in vivo CRISPR screen in primary ALL material. To that end, we took advantage of primogra

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Wang, Laidi, Wenshuang Liang, Shasha Wang, et al. "Circular RNA expression profiling reveals that circ-PLXNA1 functions in duck adipocyte differentiation." PLOS ONE 15, no. 7 (2020): e0236069. http://dx.doi.org/10.1371/journal.pone.0236069.

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8

Kotan, Leman D., Emregul Isik, Ihsan Turan, et al. "Prevalence and associated phenotypes of PLXNA1 variants in normosmic and anosmic idiopathic hypogonadotropic hypogonadism." Clinical Genetics 95, no. 2 (2018): 320–24. http://dx.doi.org/10.1111/cge.13482.

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Park, Kaylee, Laurie E. Seltzer, Emily Tuttle, Ghayda M. Mirzaa, and Alex R. Paciorkowski. "PLXNA1 developmental encephalopathy with syndromic features: A case report and review of the literature." American Journal of Medical Genetics Part A 173, no. 7 (2017): 1951–54. http://dx.doi.org/10.1002/ajmg.a.38236.

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10

Wang, Wei-Wei, Zhi-Hua Zhao, Li Wang, et al. "MicroRNA-134 prevents the progression of esophageal squamous cell carcinoma via the PLXNA1-mediated MAPK signalling pathway." EBioMedicine 46 (August 2019): 66–78. http://dx.doi.org/10.1016/j.ebiom.2019.07.050.

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11

Men, Meichao, Xinying Wang, Jiayu Wu, et al. "Prevalence and associated phenotypes of DUSP6, IL17RD and SPRY4 variants in a large Chinese cohort with isolated hypogonadotropic hypogonadism." Journal of Medical Genetics 58, no. 1 (2020): 66–72. http://dx.doi.org/10.1136/jmedgenet-2019-106786.

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BackgroundFGF8-FGFR1 signalling is involved in multiple biological processes, while impairment of this signalling is one of the main reasons for isolated hypogonadotropic hypogonadism (IHH). Recently, several negative modulators of FGF8-FGFR1 signalling were also found to be involved in IHH, including DUSP6, IL17RD, SPRY2 and SPRY4. The aim of this study was to investigate the genotypic and phenotypic spectra of these genes in a large cohort of Chinese patients with IHH.MethodsA total of 196 patients with IHH were enrolled in this study. Whole-exome sequencing was performed to identify variant

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12

Şen, Sinan, Christopher J. Lux, and Ralf Erber. "A Potential Role of Semaphorin 3A during Orthodontic Tooth Movement." International Journal of Molecular Sciences 22, no. 15 (2021): 8297. http://dx.doi.org/10.3390/ijms22158297.

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Background: Induced tooth movement during orthodontic therapy requires mechano-induced bone remodeling. Besides various cytokines and growth-factors, neuronal guidance molecules gained attention for their roles in bone homeostasis and thus, potential roles during tooth movement. Several neuronal guidance molecules have been implicated in the regulation of bone remodeling. Amongst them, Semaphorin 3A is particular interesting as it concurrently induces osteoblast differentiation and disturbs osteoclast differentiation. Methods: Mechano-regulation of Sema3A and its receptors PlexinA1 and Neuropi

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13

Wang, Wei-Wei, Zhi-Hua Zhao, Li Wang, et al. "Corrigendum to ‘MicroRNA-134 prevents the progression of esophageal squamous cell carcinoma via the PLXNA1-mediated MAPK signalling pathway’ [EBioMedicine 46 (2019) 66–78]." EBioMedicine 55 (May 2020): 102772. http://dx.doi.org/10.1016/j.ebiom.2020.102772.

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14

WANG, JUN, Bicheng Zhang, Jianguo Sun, et al. "Identification of a prognostic immune-related signature for small cell lung cancer." Journal of Clinical Oncology 38, no. 15_suppl (2020): e21041-e21041. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e21041.

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e21041 Background: As a subgroup of lung cancer, small cell lung cancer (SCLC) is characterized by a short tumor doubling time, high rates of early occurred distant cancer spread, and poor outcome. Despite its exquisite sensitivity to chemotherapy and radiotherapy, acquired drug resistance and tumor progression was impossibly avoided. This study aimed to develop a robust signature based on immune-related genes to predict the outcome of patients with SCLC. Methods: The expression data of 77 SCLC patients from George’s cohort were divided into training and testing set, and 1,534 immune-related g

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Al Amri, Waleed S., Diana E. Baxter, Andrew M. Hanby, et al. "Identification of candidate mediators of chemoresponse in breast cancer through therapy-driven selection of somatic variants." Breast Cancer Research and Treatment 183, no. 3 (2020): 607–16. http://dx.doi.org/10.1007/s10549-020-05836-7.

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Abstract Purpose More than a third of primary breast cancer patients are treated with cytotoxic chemotherapy, typically without guidance from predictive markers. Increased use of neoadjuvant chemotherapy provides opportunities for identification of molecules associated with treatment response, by comparing matched tumour samples before and after therapy. Our hypothesis was that somatic variants of increased prevalence after therapy promote resistance, while variants with reduced prevalence cause sensitivity. Methods We performed systematic analyses of matched pairs of cancer exomes from primar

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Wang, Liu, Xiangfen Li, Yao Song, Dongzhe Song, and Dingming Huang. "The emerging roles of semaphorin4D/CD100 in immunological diseases." Biochemical Society Transactions 48, no. 6 (2020): 2875–90. http://dx.doi.org/10.1042/bst20200821.

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In vertebrates, the semaphorin family of proteins is composed of 21 members that are divided into five subfamilies, i.e. classes 3 to 7. Semaphorins play crucial roles in regulating multiple biological processes, such as neural remodeling, tissue regeneration, cancer progression, and, especially, in immunological regulation. Semaphorin 4D (SEMA4D), also known as CD100, is an important member of the semaphorin family and was first characterized as a lymphocyte-specific marker. SEMA4D has diverse effects on immunologic processes, including immune cell proliferation, differentiation, activation,

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Minchin, James E. N., Ingrid Dahlman, Christopher J. Harvey, et al. "Plexin D1 determines body fat distribution by regulating the type V collagen microenvironment in visceral adipose tissue." Proceedings of the National Academy of Sciences 112, no. 14 (2015): 4363–68. http://dx.doi.org/10.1073/pnas.1416412112.

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Genome-wide association studies have implicated PLEXIN D1 (PLXND1) in body fat distribution and type 2 diabetes. However, a role for PLXND1 in regional adiposity and insulin resistance is unknown. Here we use in vivo imaging and genetic analysis in zebrafish to show that Plxnd1 regulates body fat distribution and insulin sensitivity. Plxnd1 deficiency in zebrafish induced hyperplastic morphology in visceral adipose tissue (VAT) and reduced lipid storage. In contrast, subcutaneous adipose tissue (SAT) growth and morphology were unaffected, resulting in altered body fat distribution and a reduce

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18

Valiulyte, Indre, Giedrius Steponaitis, Deimante Kardonaite, Arimantas Tamasauskas, and Arunas Kazlauskas. "A SEMA3 Signaling Pathway-Based Multi-Biomarker for Prediction of Glioma Patient Survival." International Journal of Molecular Sciences 21, no. 19 (2020): 7396. http://dx.doi.org/10.3390/ijms21197396.

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Glioma is a lethal central nervous system tumor with poor patient survival prognosis. Because of the molecular heterogeneity, it is a challenge to precisely determine the type of the tumor and to choose the most effective treatment. Therefore, novel biomarkers are essential to improve the diagnosis and prognosis of glioma tumors. Class 3 semaphorin proteins (SEMA3) play an important role in tumor biology. SEMA3 transduce their signals by using neuropilin and plexin receptors, which functionally interact with the vascular endothelial growth factor-mediated signaling pathways. Therefore, the aim

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Ragaini, Simone, Sarah Wagner, Giovanni Marconi, et al. "A Three-Gene Immune Signature Including IDO1, BIN1 and PLXNC1 Predicts Survival in Acute Myeloid Leukemia." Blood 136, Supplement 1 (2020): 35–36. http://dx.doi.org/10.1182/blood-2020-139665.

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Introduction A large body of evidence has increasingly demonstrated that the immune tumor microenvironment (TME) critically contributes to acute myeloid leukemia (AML) development. However, current AML prognostic classifications only rely on leukemia cell-intrinsic alterations and do not incorporate immunological markers referring to TME. Indoleamine 2,3-dioxygenase 1 (IDO1), which is negatively regulated by the BIN1 proto-oncogene, is a central mediator of immune tolerance in the AML TME. This study aimed to identify IDO1-interacting genes in the AML TME and to develop a prognostic immune gen

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Paap, Ricardo H., Saskia Oosterbroek, Cindy M. R. J. Wagemans, et al. "FoxO6 affects Plxna4-mediated neuronal migration during mouse cortical development." Proceedings of the National Academy of Sciences 113, no. 45 (2016): E7087—E7096. http://dx.doi.org/10.1073/pnas.1609111113.

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The forkhead transcription factor FoxO6 is prominently expressed during development of the murine neocortex. However, its function in cortical development is as yet unknown. We now demonstrate that cortical development is altered in FoxO6+/− and FoxO6−/− mice, showing migrating neurons halted in the intermediate zone. Using a FoxO6-directed siRNA approach, we substantiate the requirement of FoxO6 for a correct radial migration in the developing neocortex. Subsequent genome-wide transcriptome analysis reveals altered expression of genes involved in cell adhesion, axon guidance, and gliogenesis

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21

Wen, Haitao, Yu Lei, So-Young Eun, and Jenny P.-Y. Ting. "Plexin-A4–semaphorin 3A signaling is required for Toll-like receptor– and sepsis-induced cytokine storm." Journal of Experimental Medicine 207, no. 13 (2010): 2943–57. http://dx.doi.org/10.1084/jem.20101138.

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Plexins and semaphorins are ligand–receptor pairs that serve as guidance molecules in the nervous system and play some roles in immunity. Plexins are similar to the Toll-like receptors (TLRs) in their evolutionary conservation from flies to mammals. By studying plexin-A4–deficient (Plxna4−/−) innate immune cells, in this study we show a novel influence of plexin-A4 on TLR signaling. Plxna4−/− cells exhibit defective inflammatory cytokine production upon activation by a spectrum of TLR agonists and bacteria. Plexin-A4 is required for TLR-induced activation of the small guanosine triphosphate hy

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Wray, Naomi R., Michael R. James, Steven P. Mah, et al. "Anxiety and Comorbid Measures Associated With PLXNA2." Archives of General Psychiatry 64, no. 3 (2007): 318. http://dx.doi.org/10.1001/archpsyc.64.3.318.

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23

Schulte, Eva C., Immanuel Stahl, Darina Czamara, et al. "Rare Variants in PLXNA4 and Parkinson’s Disease." PLoS ONE 8, no. 11 (2013): e79145. http://dx.doi.org/10.1371/journal.pone.0079145.

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24

Patnaik, Mrinal M., Eric Klee, Eric D. Wieben, and David Dingli. "Genomics Of Familial Myelodysplastic Syndromes and Acute Myeloid Leukemia." Blood 122, no. 21 (2013): 2803. http://dx.doi.org/10.1182/blood.v122.21.2803.2803.

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Abstract Background The mutational landscape in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) is becoming increasingly apparent. Although some mutations and translocations occur in a substantial fraction of patients, in many, the etiologic mutations are unknown and current cytogenetic testing uninformative. Recent whole genome studies show that the mutational landscape can be very diverse. Genomic studies in families at high risk of developing MDS and AML can be highly informative in identifying potentially oncogenic mutations. We have identified a family with a high inciden

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Großkopf, Anna K., Sarah Schlagowski, Thomas Fricke, Armin Ensser, Ronald C. Desrosiers, and Alexander S. Hahn. "Plxdc family members are novel receptors for the rhesus monkey rhadinovirus (RRV)." PLOS Pathogens 17, no. 3 (2021): e1008979. http://dx.doi.org/10.1371/journal.ppat.1008979.

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The rhesus monkey rhadinovirus (RRV), a γ2-herpesvirus of rhesus macaques, shares many biological features with the human pathogenic Kaposi’s sarcoma-associated herpesvirus (KSHV). Both viruses, as well as the more distantly related Epstein-Barr virus, engage cellular receptors from the Eph family of receptor tyrosine kinases (Ephs). However, the importance of the Eph interaction for RRV entry varies between cell types suggesting the existence of Eph-independent entry pathways. We therefore aimed to identify additional cellular receptors for RRV by affinity enrichment and mass spectrometry. We

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Pecho-Vrieseling, Eline, Markus Sigrist, Yutaka Yoshida, Thomas M. Jessell, and Silvia Arber. "Specificity of sensory–motor connections encoded by Sema3e–Plxnd1 recognition." Nature 459, no. 7248 (2009): 842–46. http://dx.doi.org/10.1038/nature08000.

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Li, Rui, Xin Teng, Haicheng Zhu, Tongliang Han, and Qingwei Liu. "MiR-4500 Regulates PLXNC1 and Inhibits Papillary Thyroid Cancer Progression." Hormones and Cancer 10, no. 4-6 (2019): 150–60. http://dx.doi.org/10.1007/s12672-019-00366-1.

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Pijuan, Jordi, Juan Darío Ortigoza‐Escobar, Juan Ortiz, et al. "PLXNA2 and LRRC40 as candidate genes in autism spectrum disorder." Autism Research 14, no. 6 (2021): 1088–100. http://dx.doi.org/10.1002/aur.2502.

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29

Sheu, Chau-Chyun, Wei-An Chang, Ming-Ju Tsai, Ssu-Hui Liao, Inn-Wen Chong, and Po-Lin Kuo. "Gene Expression Changes Associated with Nintedanib Treatment in Idiopathic Pulmonary Fibrosis Fibroblasts: A Next-Generation Sequencing and Bioinformatics Study." Journal of Clinical Medicine 8, no. 3 (2019): 308. http://dx.doi.org/10.3390/jcm8030308.

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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal interstitial lung disease. Therapeutic options for IPF remain limited. Nintedanib, a tyrosine kinase inhibitor approved for IPF treatment, is known to inhibit fibroblasts proliferation, migration and transformation to myofibroblasts. However, how nintedanib changes gene regulations in IPF has never been systematically investigated. We conducted a next-generation sequencing and bioinformatics study to evaluate the changes of mRNA and miRNA profiles in IPF fibroblasts treated with 2 µM and 4 µM nintedanib, compared to those

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Ragaini, Simone, Sarah Wagner, Giovanni Marconi, et al. "An IDO1-Related 3-Gene Signature Predicts Overall Survival in Intermediate-Risk Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 5193. http://dx.doi.org/10.1182/blood-2019-128348.

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Introduction: ELN intermediate-risk AML poses considerable challenges to clinicians both in terms of accurate prognostication and optimal treatment. Indoleamine 2,3-dioxygenase 1 (IDO1) plays a central role as a mediator of immune tolerance in AML through the increase of Treg cells. IDO1 activity is negatively regulated by the BIN1 proto-oncogene. Herein, we analyzed the correlation between BIN1 and IDO1 expression in AML, also focusing on IDO1-interacting genes, with the aim to identify a predictive gene signature for OS. Methods: Biological and clinical data of 732 patients with de novo AML

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Wang, Hui, Fu-Rong Sun, Lin Tan, et al. "Association study of the PLXNA4 gene with the risk of Alzheimer’s disease." Annals of Translational Medicine 4, no. 6 (2016): 108. http://dx.doi.org/10.21037/atm.2016.03.23.

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Zygmunt, Tomasz, Carl M. Gay, Jordan Blondelle, et al. "Beyond guidance: A novel role for Sema–PlxnD1 signaling in vascular development." Developmental Biology 356, no. 1 (2011): 102. http://dx.doi.org/10.1016/j.ydbio.2011.05.009.

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Garcia, Alix, Sylvie Dunoyer-Geindre, Veronika Zapilko, Séverine Nolli, Jean-Luc Reny, and Pierre Fontana. "Functional Validation of microRNA-126-3p as a Platelet Reactivity Regulator Using Human Haematopoietic Stem Cells." Thrombosis and Haemostasis 119, no. 02 (2019): 254–63. http://dx.doi.org/10.1055/s-0038-1676802.

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Background Platelets are an abundant source of micro-ribonucleic acids (miRNAs) that may play a role in the regulation of platelet function. Some miRNAs, such as miR-126-3p, have been noted as potential biomarkers of platelet reactivity and the recurrence of cardiovascular events. However, the biological relevance of these associations remains uncertain, and the functional validation of candidate miRNAs on human-derived cells is lacking. Objective This article functionally validates miR-126-3p as a regulator of platelet reactivity in platelet-like structures (PLS) derived from human haematopoi

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Takeshita, Mizuho, Kazuo Yamada, Eiji Hattori, et al. "Genetic examination of the PLXNA2 gene in Japanese and Chinese people with schizophrenia." Schizophrenia Research 99, no. 1-3 (2008): 359–64. http://dx.doi.org/10.1016/j.schres.2007.11.002.

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Hamm, Mailin Julia, Bettina Carmen Kirchmaier, and Wiebke Herzog. "Sema3d controls collective endothelial cell migration by distinct mechanisms via Nrp1 and PlxnD1." Journal of Cell Biology 215, no. 3 (2016): 415–30. http://dx.doi.org/10.1083/jcb.201603100.

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During cardiovascular development, tight spatiotemporal regulation of molecular cues is essential for controlling endothelial cell (EC) migration. Secreted class III Semaphorins play an important role in guidance of neuronal cell migration and were lately linked to regulating cardiovascular development. Recently, SEMA3D gene disruptions were associated with cardiovascular defects in patients; however, the mechanisms of action were not revealed. Here we show for the first time that Sema3d regulates collective EC migration in zebrafish through two separate mechanisms. Mesenchymal Sema3d guides o

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Mah, S., M. R. Nelson, L. E. DeLisi, et al. "Identification of the semaphorin receptor PLXNA2 as a candidate for susceptibility to schizophrenia." Molecular Psychiatry 11, no. 5 (2006): 471–78. http://dx.doi.org/10.1038/sj.mp.4001785.

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Qureshi, Moaz, Mohamed Hatem, Raed Alroughani, Sindhu P. Jacob, and Rabeah Abbas Al-Temaimi. "PLXNA3 Variant rs5945430 is Associated with Severe Clinical Course in Male Multiple Sclerosis Patients." NeuroMolecular Medicine 19, no. 2-3 (2017): 286–92. http://dx.doi.org/10.1007/s12017-017-8443-0.

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Qian, Yue-Wei, Eleanor Erikson, and James L. Maller. "Mitotic Effects of a Constitutively Active Mutant of the Xenopus Polo-Like Kinase Plx1." Molecular and Cellular Biology 19, no. 12 (1999): 8625–32. http://dx.doi.org/10.1128/mcb.19.12.8625.

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ABSTRACT During mitosis the Xenopus polo-like kinase 1 (Plx1) plays key roles in the activation of Cdc25C, in spindle assembly, and in cyclin B degradation. Previous work has shown that the activation of Plx1 requires phosphorylation on serine and threonine residues. In the present work, we demonstrate that replacement of Ser-128 or Thr-201 with a negatively charged aspartic acid residue (S128D or T201D) elevates Plx1 activity severalfold and that replacement of both Ser-128 and Thr-201 with Asp residues (S128D/T201D) increases Plx1 activity approximately 40-fold. Microinjection of mRNA encodi

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Qian, Yue-Wei, Eleanor Erikson, Chuan Li, and James L. Maller. "Activated Polo-Like Kinase Plx1 Is Required at Multiple Points during Mitosis in Xenopus laevis." Molecular and Cellular Biology 18, no. 7 (1998): 4262–71. http://dx.doi.org/10.1128/mcb.18.7.4262.

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ABSTRACT Entry into mitosis depends upon activation of the dual-specificity phosphatase Cdc25C, which dephosphorylates and activates the cyclin B-Cdc2 complex. Previous work has shown that the Xenopuspolo-like kinase Plx1 can phosphorylate and activate Cdc25C in vitro. In the work presented here, we demonstrate that Plx1 is activated in vivo during oocyte maturation with the same kinetics as Cdc25C. Microinjection of wild-type Plx1 into Xenopus oocytes accelerated the rate of activation of Cdc25C and cyclin B-Cdc2. Conversely, microinjection of either an antibody against Plx1 or kinase-dead Pl

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Wang, Zhiqiong, Xiaochuan Wang, Hongying Zhou, Xiao Dan, Lixiang Jiang, and Yifei Wu. "Long non-coding RNA CASC2 inhibits tumorigenesis via the miR-181a/PLXNC1 axis in melanoma." Acta Biochimica et Biophysica Sinica 50, no. 3 (2018): 263–72. http://dx.doi.org/10.1093/abbs/gmx148.

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Fujii, Takashi, Yoshimi Iijima, Hitomi Kondo, et al. "Failure to confirm an association between the PLXNA2 gene and schizophrenia in a Japanese population." Progress in Neuro-Psychopharmacology and Biological Psychiatry 31, no. 4 (2007): 873–77. http://dx.doi.org/10.1016/j.pnpbp.2007.01.027.

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Tian, T. V., N. Tomavo, L. Huot, et al. "Identification of novel TMPRSS2:ERG mechanisms in prostate cancer metastasis: involvement of MMP9 and PLXNA2." Oncogene 33, no. 17 (2013): 2204–14. http://dx.doi.org/10.1038/onc.2013.176.

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Vreeken, D., C. S. Bruikman, H. Zhang, A. J. van Zonneveld, G. K. Hovingh, and J. van Gils. "Downregulation Of Endothelial Plxna4 Under Pro-Atherosclerotic Conditions Diminishes Vascular Integrity Enabling Monocyte Transendothelial Migration." Atherosclerosis 287 (August 2019): e97. http://dx.doi.org/10.1016/j.atherosclerosis.2019.06.282.

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Abrieu, A., T. Brassac, S. Galas, D. Fisher, J. C. Labbe, and M. Doree. "The Polo-like kinase Plx1 is a component of the MPF amplification loop at the G2/M-phase transition of the cell cycle in Xenopus eggs." Journal of Cell Science 111, no. 12 (1998): 1751–57. http://dx.doi.org/10.1242/jcs.111.12.1751.

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We have investigated whether Plx1, a kinase recently shown to phosphorylate cdc25c in vitro, is required for activation of cdc25c at the G2/M-phase transition of the cell cycle in Xenopus. Using immunodepletion or the mere addition of an antibody against the C terminus of Plx1, which suppressed its activation (not its activity) at G2/M, we show that Plx1 activity is required for activation of cyclin B-cdc2 kinase in both interphase egg extracts receiving recombinant cyclin B, and cycling extracts that spontaneously oscillate between interphase and mitosis. Furthermore, a positive feedback loop

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Wong, Oi Kwan, and Guowei Fang. "Plx1 is the 3F3/2 kinase responsible for targeting spindle checkpoint proteins to kinetochores." Journal of Cell Biology 170, no. 5 (2005): 709–19. http://dx.doi.org/10.1083/jcb.200502163.

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Dynamic attachment of microtubules to kinetochores during mitosis generates pulling force, or tension, required for the high fidelity of chromosome separation. A lack of tension activates the spindle checkpoint and delays the anaphase onset. A key step in the tension–response pathway involves the phosphorylation of the 3F3/2 epitope by an unknown kinase on untensed kinetochores. Using a rephosphorylation assay in Xenopus laevis extracts, we identified the kinetochore-associated Polo-like kinase Plx1 as the kinase both necessary and sufficient for this phosphorylation. Indeed, Plx1 is the physi

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Wong, Oi Kwan, and Guowei Fang. "Cdk1 phosphorylation of BubR1 controls spindle checkpoint arrest and Plk1-mediated formation of the 3F3/2 epitope." Journal of Cell Biology 179, no. 4 (2007): 611–17. http://dx.doi.org/10.1083/jcb.200708044.

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Accurate chromosome segregation is controlled by the spindle checkpoint, which senses kinetochore– microtubule attachments and tension across sister kinetochores. An important step in the tension-signaling pathway involves the phosphorylation of an unknown protein by polo-like kinase 1/Xenopus laevis polo-like kinase 1 (Plx1) on kinetochores lacking tension to generate the 3F3/2 phosphoepitope. We report here that the checkpoint protein BubR1 interacts with Plx1 and that phosphorylation of BubR1 by Plx1 generates the 3F3/2 epitope. Formation of the BubR1 3F3/2 epitope by Plx1 requires a prior

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Qian, Yue-Wei, Eleanor Erikson, Frédéric E. Taieb, and James L. Maller. "The Polo-like Kinase Plx1 Is Required for Activation of the Phosphatase Cdc25C and Cyclin B-Cdc2 in Xenopus Oocytes." Molecular Biology of the Cell 12, no. 6 (2001): 1791–99. http://dx.doi.org/10.1091/mbc.12.6.1791.

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In the Xenopus oocyte system mitogen treatment triggers the G2/M transition by transiently inhibiting the cAMP-dependent protein kinase (PKA); subsequently, other signal transduction pathways are activated, including the mitogen-activated protein kinase (MAPK) and polo-like kinase pathways. To study the interactions between these pathways, we have utilized a cell-free oocyte extract that carries out the signaling events of oocyte maturation after addition of the heat-stable inhibitor of PKA, PKI. PKI stimulated the synthesis of Mos and activation of both the MAPK pathway and the Plx1/Cdc25C/cy

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Ebert, A. M., S. J. Childs, C. L. Hehr, P. B. Cechmanek, and S. McFarlane. "Sema6a and Plxna2 mediate spatially regulated repulsion within the developing eye to promote eye vesicle cohesion." Development 141, no. 12 (2014): 2473–82. http://dx.doi.org/10.1242/dev.103499.

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Jun, Gyungah, Hirohide Asai, Elodie Drapeau, et al. "O4-06-02: Genetic variation in PLXNA4 associated with susceptibility of Alzheimer's disease through tau phosphorylation." Alzheimer's & Dementia 9 (July 2013): P692. http://dx.doi.org/10.1016/j.jalz.2013.04.366.

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Hwang, J. Y., J. Y. Lee, M. H. Park, et al. "Association of PLXNA2 polymorphisms with vertebral fracture risk and bone mineral density in postmenopausal Korean population." Osteoporosis International 17, no. 11 (2006): 1592–601. http://dx.doi.org/10.1007/s00198-006-0126-x.

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