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Growth and cortical microtubule dynamics in shoot organs under microgravity and hypergravity conditions
Kazuyuki Wakabayashi,Kouichi Soga,Takayuki Hoson
- , 2018, DOI: 10.1080/15592324.2017.1422468
Abstract: The body shape of plants varied in proportion to the logarithm of the magnitude of gravity in the range from microgravity to hypergravity to resist the gravitational force. Here we discuss the roles of cortical microtubule and 65 kDa microtubule-associated protein-1 (MAP65-1) in gravity-induced modification of growth anisotropy. Microgravity stimulated elongation growth and suppressed lateral expansion in shoot organs, such as hypocotyls and epicotyls. On the other hand, hypergravity inhibited elongation growth and promoted lateral expansion in shoot organs. The number of cells with transverse microtubules was increased by microgravity, but decreased by hypergravity. Furthermore, the levels of MAP65-1, which is involved in the maintenance of the transverse microtubule orientation, were increased by microgravity, but decreased by hypergravity. Therefore, the regulation of orientation of cortical microtubules via changes in the levels of MAP65-1 may contribute to the modification of the body shape of plants to resist the gravitational force
JWA protein binds to α-tubulin in PC 12 cells
Hairong Chen,Aiqun Li,Aiping Li,Jianwei Zhou
Chinese Science Bulletin , 2004, DOI: 10.1007/BF02900966
Abstract: Our previous study elucidated that JWA protein was a newly identified microtubule-associated protein (MAP), which combined to and co-localized with β-tubulin. In the present study, we designed a series of experiments to explore if any interactions between JWA protein and α-tubulin existed and how JWA protein would functionally link to α-tubulin, especially in cell mitosis. Results of coimmunoprecipitation, gene transfection and immunofluorescence microscopy from PC12 and HEK293 cells provided strong evidence for a linkage between JWA protein and α-tubulin. Our data showed that JWA protein bound to α-tubulin stably no matter whether α-tubulin was polymerized or not. In addition, by using antisense oligonucleotides, cell cycle blocking agents and hypothermia disposal techniques, we also found the interaction between JWA protein and α-tubulin. The further analysis using flow cytometry and confocal microscopy showed that both proteins co-existed in PC12 cells and were independent on the cell cycle. In conclusion, JWA protein is a newly identified microtubuleassociated protein, binds to α-tubulin, and probably plays an important role in regulation of microtubular stability.
JWA protein binds to a-tubulin in PC12 cells
JWA protein binds to α-tubulin in PC12 cells
CHEN Hairong,LI Aiqun,LI Aiping,ZHOU Jianwei,
CHENHairong,LIAiqun,LIAiping,ZHOUJianwei
科学通报(英文版) , 2004,
Abstract: Our previous study elucidated that JWA protein was a newly identified microtubule-associated protein (MAP), which combined to and co-localized with β-tubulin. In the present study, we designed a series of experiments to explore if any interactions between JWA protein and α-tubulin existed and how JWA protein would functionally link to α-tubulin, especially in cell mitosis. Results of coimmunoprecipitation, gene transfection and immunofluorescence microscopy from PC12 and HEK293 cells provided strong evidence for a linkage between JWA protein and α-tubulin. Our data showed that JWA protein bound to α-tubulin stably no matter whether α-tubulin was polymerized or not. In addition, by using antisense oligonucleotides, cell cycle blocking agents and hypothermia disposal techniques, we also found the interaction between JWA protein and α-tubulin. The further analysis using flow cytometry and confocal microscopy showed that both proteins co-existed in PC12 cells and were independent on the cell cycle. In conclusion, JWA protein is a newly identified microtubuleassociated protein, binds to α-tubulin, and probably plays an important role in regulation of microtubular stability.
A Mutation in Mtap2 Is Associated with Arrest of Mammalian Spermatocytes before the First Meiotic Division
Fengyun Sun,Mary Ann Handel
Genes , 2011, DOI: 10.3390/genes2010021
Abstract: In spite of evolutionary conservation of meiosis, many of the genes that control mammalian meiosis are still unknown. We report here that the ENU-induced repro4 mutation, identified in a screen to uncover genes that control mouse meiosis, causes failure of spermatocytes to exit meiotic prophase I via the G2/MI transition. Major events of meiotic prophase I occurred normally in affected spermatocytes and known regulators of the meiotic G2/MI transition were present and functional. Deep sequencing of mutant DNA revealed a mutation located in an intron of the Mtap2 gene, encoding microtubule-associated protein 2, and levels of Mtap2 transcript were reduced in mutant testes. This evidence implicates MTAP2 as required directly or indirectly for completion of meiosis and normal spermatogenesis in mammals.
Genetics of frontotemporal lobar degeneration
Aswathy P,Jairani P,Mathuranath P
Annals of Indian Academy of Neurology , 2010,
Abstract: Frontotemporal lobar degeneration (FTLD) is a highly heterogenous group of progressive neurodegenerative disorders characterized by atrophy of prefrontal and anterior temporal cortices. Recently, the research in the field of FTLD has gained increased attention due to the clinical, neuropathological, and genetic heterogeneity and has increased our understanding of the disease pathogenesis. FTLD is a genetically complex disorder. It has a strong genetic basis and 50% of patients show a positive family history for FTLD. Linkage studies have revealed seven chromosomal loci and a number of genes including MAPT, PGRN, VCP, and CHMB-2B are associated with the disease. Neuropathologically, FTLD is classified into tauopathies and ubiquitinopathies. The vast majority of FTLD cases are characterized by pathological accumulation of tau or TDP-43 positive inclusions, each as an outcome of mutations in MAPT or PGRN, respectively. Identification of novel proteins involved in the pathophysiology of the disease, such as progranulin and TDP-43, may prove to be excellent biomarkers of disease progression and thereby lead to the development of better therapeutic options through pharmacogenomics. However, much more dissections into the causative pathways are needed to get a full picture of the etiology. Over the past decade, advances in research on the genetics of FTLD have revealed many pathogenic mutations leading to different clinical manifestations of the disease. This review discusses the current concepts and recent advances in our understanding of the genetics of FTLD.
Phosphorylation of different tau sites during progression of Alzheimer’s disease
Bianca Kerschbaumer,Birgit Hutter-Paier,Christina Hoeller,Guenther Daum,Joerg Neddens,Johannes Attems,Magdalena Temmel,Stefanie Flunkert,Tina Loeffler,Vera Niederkofler
- , 2018, DOI: 10.1186/s40478-018-0557-6
Abstract: The online version of this article (10.1186/s40478-018-0557-6) contains supplementary material, which is available to authorized users
EML4-ALK Variants: Biological and Molecular Properties, and the Implications for Patients
George Jackson,Richard Bayliss,Sarah R. Sabir,Sharon Yeoh
- , 2017, DOI: 10.3390/cancers9090118
Abstract: Since the discovery of the fusion between EML4 (echinoderm microtubule associated protein-like 4) and ALK (anaplastic lymphoma kinase), EML4-ALK, in lung adenocarcinomas in 2007, and the subsequent identification of at least 15 different variants in lung cancers, there has been a revolution in molecular-targeted therapy that has transformed the outlook for these patients. Our recent focus has been on understanding how and why the expression of particular variants can affect biological and molecular properties of cancer cells, as well as identifying the key signalling pathways triggered, as a result. In the clinical setting, this understanding led to the discovery that the type of variant influences the response of patients to ALK therapy. Here, we discuss what we know so far about the EML4-ALK variants in molecular signalling pathways and what questions remain to be answered. In the longer term, this analysis may uncover ways to specifically treat patients for a better outcome
Morphological alterations induced by the exposure to TiO2 nanoparticles in primary cortical neuron cultures and in the brain of rats
Annica Frau,Denis Nonclercq,Dimitri Stanicki,Laurence Ris,Pascaline Rugira,Paula Paci,Pauline Deneufbourg,Sophie Laurent,Xavier Valentini
- , 2018, DOI: 10.1016/j.toxrep.2018.08.006
Abstract:
Targeted human cytolytic fusion proteins at the cutting edge: harnessing the apoptosis-inducing properties of human enzymes for the selective elimination of tumor cells
Krupa Naran,Neelakshi Mungra,Precious Hlongwane,Sandra Jordaan,Shivan Chetty,Stefan Barth
- , 2019, DOI: 10.18632/oncotarget.26618
Abstract: Patient-specific targeted therapy represents the holy grail of anti-cancer therapeutics, allowing potent tumor depletion without detrimental off-target toxicities. Disease-specific monoclonal antibodies have been employed to bind to oncogenic cell-surface receptors, representing the earliest form of immunotherapy. Targeted drug delivery was first achieved by means of antibody-drug conjugates, which exploit the differential expression of tumor-associated antigens as a guiding mechanism for the specific delivery of chemically-conjugated chemotherapeutic agents to diseased target cells. Biotechnological advances have expanded the repertoire of immunology-based tumor-targeting strategies, also paving the way for the next intuitive step in targeted drug delivery: the construction of recombinant protein drugs consisting of an antibody-based targeting domain genetically fused with a cytotoxic peptide, known as an immunotoxin. However, the most potent protein toxins have typically been derived from bacterial or plant virulence factors and commonly feature both off-target toxicity and immunogenicity in human patients. Further refinement of immunotoxin technology thus led to the replacement of monoclonal antibodies with humanized antibody derivatives, including the substitution of non-human toxic peptides with human cytolytic proteins. Preclinically tested human cytolytic fusion proteins (hCFPs) have proven promising as non-immunogenic combinatory anti-cancer agents, however they still require further enhancement to achieve convincing candidacy as a single-mode therapeutic. To date, a portfolio of highly potent human toxins has been established; ranging from microtubule-associated protein tau (MAP tau), RNases, granzyme B (GrB) and death-associated protein kinase (DAPk). In this review, we discuss the most recent findings on the use of these apoptosis-inducing hCFPs for the treatment of various cancers
Neural differentiation of choroid plexus epithelial cells: role of human traumatic cerebrospinal fluid
Abbas Aliaghaei,Abbas Piryaei,Abdollah Amini,Afsoun Seddighi,Elham Hashemi,Fatemeh Shaerzadeh,Mehdi Eskandarian Broujeni,Ramin Pouriran,Yousef Sadeghi
- , 2017, DOI: 10.4103/1673-5374.198989
Abstract: Author contributions: YS and Aliaghaei A conceived and designed the experiments. EH performed the experiments. Amini A, MEB, and YS analyzed the data. AS, AP, and Amini A contributed to reagents/materials/analysis tools. Aliaghaei A, FS and RP wrote the paper. All authors approved the final version of this paper
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