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Автор: Grafiati

Опубліковано: 6 вересня 2023

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1

Horn, Zachi, Hourinaz Behesti, and Mary E. Hatten. "N-cadherin provides a cis and trans ligand for astrotactin that functions in glial-guided neuronal migration." Proceedings of the National Academy of Sciences 115, no. 42 (September 27, 2018): 10556–63. http://dx.doi.org/10.1073/pnas.1811100115.

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Prior studies demonstrate that astrotactin (ASTN1) provides a neuronal receptor for glial-guided CNS migration. Here we report that ASTN1 binds N-cadherin (CDH2) and that the ASTN1:CDH2 interaction supports cell–cell adhesion. To test the function of ASTN1:CDH2 binding in glial-guided neuronal migration, we generated a conditional loss of Cdh2 in cerebellar granule cells and in glia. Granule cell migration was slowed in cerebellar slice cultures after a conditional loss of neuronal Cdh2, and more severe migration defects occurred after a conditional loss of glial Cdh2. Expression in granule cells of a mutant form of ASTN1 that does not bind CDH2 also slowed migration. Moreover, in vitro chimeras of granule cells and glia showed impaired neuron–glia attachment in the absence of glial, but not neuronal, Cdh2. Thus, cis and trans bindings of ASTN1 to neuronal and glial CDH2 form an asymmetric neuron–glial bridge complex that promotes glial-guided neuronal migration.

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2

Behesti, Hourinaz, Taylor R. Fore, Peter Wu, Zachi Horn, Mary Leppert, Court Hull, and Mary E. Hatten. "ASTN2 modulates synaptic strength by trafficking and degradation of surface proteins." Proceedings of the National Academy of Sciences 115, no. 41 (September 21, 2018): E9717—E9726. http://dx.doi.org/10.1073/pnas.1809382115.

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Surface protein dynamics dictate synaptic connectivity and function in neuronal circuits. ASTN2, a gene disrupted by copy number variations (CNVs) in neurodevelopmental disorders, including autism spectrum, was previously shown to regulate the surface expression of ASTN1 in glial-guided neuronal migration. Here, we demonstrate that ASTN2 binds to and regulates the surface expression of multiple synaptic proteins in postmigratory neurons by endocytosis, resulting in modulation of synaptic activity. In cerebellar Purkinje cells (PCs), by immunogold electron microscopy, ASTN2 localizes primarily to endocytic and autophagocytic vesicles in the cell soma and in subsets of dendritic spines. Overexpression of ASTN2 in PCs, but not of ASTN2 lacking the FNIII domain, recurrently disrupted by CNVs in patients, including in a family presented here, increases inhibitory and excitatory postsynaptic activity and reduces levels of ASTN2 binding partners. Our data suggest a fundamental role for ASTN2 in dynamic regulation of surface proteins by endocytic trafficking and protein degradation.

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3

Chang, Hao, Philip M. Smallwood, John Williams, and Jeremy Nathans. "Intramembrane Proteolysis of Astrotactins." Journal of Biological Chemistry 292, no. 8 (January 18, 2017): 3506–16. http://dx.doi.org/10.1074/jbc.m116.768077.

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Astrotactins are vertebrate-specific membrane proteins implicated in neuron-glia interactions during central nervous system development and in hair follicle polarity during skin development. By studying epitope-tagged derivatives of mouse astrotactin-2 (Astn2) produced in transfected cells, we determined that the amino and carboxyl termini reside in the extracellular space and are initially linked by two transmembrane segments and a single cytoplasmic domain. We further show that Astn2 undergoes proteolytic cleavage in the second transmembrane domain (TM2) and that a disulfide bond holds the resulting two fragments together. Recombinant Astn1 also undergoes TM2 cleavage, as does Astn2 isolated from mouse cerebellum. Astn2 intramembrane proteolysis is insensitive to replacement of TM2 by the transmembrane domain of CD74 or by 21 alanines. However, replacement of TM2 by the transmembrane domain of CD4, the asialoglycoprotein receptor, or the transferrin receptor eliminates intramembrane proteolysis, as does leucine substitution of residues that overlap or are immediately upstream of the cleavage site. Replacement of the transmembrane domain of CD74 or the asialoglycoprotein receptor with Astn2 TM2 leads to the appearance of a carboxyl-terminal fragment consistent with intramembrane proteolysis. These experiments define a highly unusual transmembrane topology for the astrotactins, reveal intramembrane proteolysis as a feature of astrotactin maturation, and constrain the substrate sequences that are permissive for cleavage of one type 2 transmembrane segment.

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4

Wilson, P. M., R. H. Fryer, Y. Fang, and M. E. Hatten. "Astn2, A Novel Member of the Astrotactin Gene Family, Regulates the Trafficking of ASTN1 during Glial-Guided Neuronal Migration." Journal of Neuroscience 30, no. 25 (June 23, 2010): 8529–40. http://dx.doi.org/10.1523/jneurosci.0032-10.2010.

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5

McDougall, Annie R. A., Vanny Wiradjaja, Aminath Azhan, Anqi Li, Nadia Hale, Mary E. Wlodek, Stuart B. Hooper, Megan J. Wallace, and Mary Tolcos. "Intrauterine Growth Restriction Alters the Postnatal Development of the Rat Cerebellum." Developmental Neuroscience 39, no. 1-4 (2017): 215–27. http://dx.doi.org/10.1159/000470902.

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Intrauterine growth restriction (IUGR) is a major cause of antenatal brain injury. We aimed to characterize cerebellar deficits following IUGR and to investigate the potential underlying cellular and molecular mechanisms. At embryonic day 18, pregnant rats underwent either sham surgery (controls; n = 23) or bilateral uterine vessel ligation to restrict blood flow to fetuses (IUGR; n = 20). Offspring were collected at postnatal day 2 (P2), P7, and P35. Body weights were reduced at P2, P7, and P35 in IUGR offspring (p < 0.05) compared with controls. At P7, the width of the external granule layer (EGL) was 30% greater in IUGR than control rats (p < 0.05); there was no difference in the width of the proliferative zone or in the density of Ki67-positive cells in the EGL. Bergmann glia were disorganized at P7 and P35 in IUGR pups, and by P35, there was a 10% decrease in Bergmann glial fiber density (p < 0.05) compared with controls. At P7, trophoblast antigen-2 (Trop2) mRNA and protein levels in the cerebellum were decreased by 88 and 40%, respectively, and astrotactin 1 mRNA levels were increased by 20% in the IUGR rats (p < 0.05) compared with controls; there was no difference in ASTN1 protein. The expressions of other factors known to regulate cerebellar development (astrotactin 2, brain-derived neurotrophic factor, erb-b2 receptor tyrosine kinase 4, neuregulin 1, sonic hedgehog and somatostatin) were not different between IUGR and control rats at P7 or P35. These data suggest that damage to the migratory scaffold (Bergmann glial fibers) and alterations in the genes that influence migration (Trop2 and Astn1) may underlie the deficits in postnatal cerebellar development following IUGR.

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6

Hill, Shirley Y., Daniel E. Weeks, Bobby L. Jones, Nicholas Zezza, and Scott Stiffler. "ASTN1 and alcohol dependence: Family-based association analysis in multiplex alcohol dependence families." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 159B, no. 4 (April 9, 2012): 445–55. http://dx.doi.org/10.1002/ajmg.b.32048.

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7

Yi, Sheng, Shanshan Wang, Qing Zhao, Chun Yao, Yun Gu, Jie Liu, Xiaosong Gu, and Shiying Li. "miR-sc3, a Novel MicroRNA, Promotes Schwann Cell Proliferation and Migration by Targeting Astn1." Cell Transplantation 25, no. 5 (May 2016): 973–82. http://dx.doi.org/10.3727/096368916x690520.

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8

Fan, Chunli, Quanfu Ma, Xufeng Wu, Xuan Dai, Qiuzi Peng, and Hongning Cai. "Detection of DNA Methylation in Gene Loci ASTN1, DLX1, ITGA4, RXFP3, SOX17, and ZNF671 for Diagnosis of Cervical Cancer." Cancer Management and Research Volume 15 (July 2023): 635–44. http://dx.doi.org/10.2147/cmar.s417877.

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9

Amaya-Ramirez, Diego, Laura Camila Martinez-Enriquez, and Carlos Parra-López. "Usefulness of Docking and Molecular Dynamics in Selecting Tumor Neoantigens to Design Personalized Cancer Vaccines: A Proof of Concept." Vaccines 11, no. 7 (June 29, 2023): 1174. http://dx.doi.org/10.3390/vaccines11071174.

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Personalized cancer vaccines based on neoantigens are a new and promising treatment for cancer; however, there are still multiple unresolved challenges to using this type of immunotherapy. Among these, the effective identification of immunogenic neoantigens stands out, since the in silico tools used generate a significant portion of false positives. Inclusion of molecular simulation techniques can refine the results these tools produce. In this work, we explored docking and molecular dynamics to study the association between the stability of peptide–HLA complexes and their immunogenicity, using as a proof of concept two HLA-A2-restricted neoantigens that were already evaluated in vitro. The results obtained were in accordance with the in vitro immunogenicity, since the immunogenic neoantigen ASTN1 remained bound at both ends to the HLA-A2 molecule. Additionally, molecular dynamic simulation suggests that position 1 of the peptide has a more relevant role in stabilizing the N-terminus than previously proposed. Likewise, the mutations may have a “delocalized” effect on the peptide–HLA interaction, which means that the mutated amino acid influences the intensity of the interactions of distant amino acids of the peptide with the HLA. These findings allow us to propose the inclusion of molecular simulation techniques to improve the identification of neoantigens for cancer vaccines.

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10

Wang, Zhi, Cheng Feng, Hao Liu, Tian Meng, Wei-Qing Huang, Ke-Xin Song, and You-Bin Wang. "Exosomes from circ-Astn1-modified adipose-derived mesenchymal stem cells enhance wound healing through miR-138-5p/SIRT1/FOXO1 axis regulation." World Journal of Stem Cells 14, no. 10 (October 26, 2022): 777–90. http://dx.doi.org/10.4252/wjsc.v14.i10.777.

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11

Wang, Zhi, Cheng Feng, Hao Liu, Tian Meng, Wei-Qing Huang, Ke-Xin Song, and You-Bin Wang. "Exosomes from circ-Astn1-modified adipose-derived mesenchymal stem cells enhance wound healing through miR-138-5p/SIRT1/FOXO1 axis regulation." World Journal of Stem Cells 15, no. 5 (May 26, 2023): 476–89. http://dx.doi.org/10.4252/wjsc.v15.i5.476.

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12

Ghazavi, Farzaneh, Barbara De Moerloose, Wouter Van Loocke, Annelynn Wallaert, Alina Ferster, Marleen Bakkus, Genevieve Plat, et al. "Unique Long Non-Coding RNA Expression Signature in ETV6/RUNX1-Driven B-Cell Precursor Acute Lymphoblastic Leukemia." Blood 128, no. 22 (December 2, 2016): 3920. http://dx.doi.org/10.1182/blood.v128.22.3920.3920.

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Abstract Emerging evidence suggests that long non-coding RNAs (lncRNAs) are critically involved in a variety of human tumor entities and the identification of cancer-associated lncRNAs might reveal new prognostic biomarkers or novel therapeutic targets for the treatment of human cancer. In this study, we characterized the lncRNA expression signature associated with ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL), one of the most prevalent genetic subtypes of childhood leukemia. First, we used primary leukemia patient samples to identify an ETV6/RUNX1 specific expression signature consisting of 596 lncRNA transcripts. Besides using primary BCP-ALL patient samples, we also integrated these lncRNA expression data with RNA sequencing results from a panel of human BCP-ALL leukemia cell lines and identified a unique lncRNA expression profile of 16 lncRNAs exclusively associated with the presence of the ETV6/RUNX1 fusion protein. Notably, lnc-SARDH-1 (also known as DBH-AS1) was the only lncRNA from this list for which an oncogenic role has previously been postulated. Given that previous studies revealed putative overlap between lncRNA expression and the presence of regulatory enhancer elements, we also evaluated the distribution of H3K27ac, a histone modification associated with enhancer activity, at the genomic loci of the 16 ETV6/RUNX1 specific lncRNAs mentioned above. Notably, broad H3K27ac binding was identified for lnc-NKX2-3-1, lnc-RTN4R-1, lnc-GIP-1, lnc-LRP8-3, lnc-TCF12-2, lnc- C8orf4-1, lnc-C8orf4-2, lnc-TINAGL1-1 and lnc-LSM11-4 in ETV6/RUNX1-positive REH cells, whereas more discrete H3K27ac peaks were identified at putative promoter regions for lnc-TIMM21-5 and lnc-CPT2-7. Interestingly, coding genes adjacent to some of these lncRNAs showed unique overexpression in ETV6/RUNX1-positive BCP-ALLs, suggesting a possible cis regulatory relationship between these lncRNAs and their nearby protein coding genes. Finally, we applied shRNA-mediated silencing of endogenous ETV6/RUNX1, integrated these expression profiles with the patient and cell line data, to show that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 were the only lncRNAs that were truly regulated by the oncogenic fusion protein. Interestingly, subsequent lncRNA modulation experiments using LNA GapmeR technology revealed that lnc-TIMM21-5 and lnc-ASTN1-1 modulation has no effect on overall transcription, suggesting that these lncRNAs might act at the translational level or/and at various steps of mRNA processing. In contrast, lnc-NKX2-3-1 and lnc-RTN4R-1 perturbations resulted in severe changes in gene expression, suggesting an alternative mechanism of action for these lncRNAs that is more transcriptionally oriented. Most notably, loss of lnc-RTN4R-1expression significantly affected part of the ETV6/RUNX1-specific mRNA expression signature as exemplified by reduced levels of AK7, PTPRKand GBA3. Altogether, our study identified a panel of ETV6/RUNX1 specific lncRNAs that might be implicated in the biology of human BCP-ALL and could serve as novel biomarkers or novel therapeutic targets for the treatment of this prevalent subtype of human leukemia. TLM and PVV are shared last authors Disclosures No relevant conflicts of interest to declare.

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13

Cowley, Allen W., Chun Yang, Vikash Kumar, Jozef Lazar, Howard Jacob, Aron M. Geurts, Pengyuan Liu, Alex Dayton, Theresa Kurth, and Mingyu Liang. "Pappa2 is linked to salt-sensitive hypertension in Dahl S rats." Physiological Genomics 48, no. 1 (January 2016): 62–72. http://dx.doi.org/10.1152/physiolgenomics.00097.2015.

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A 1.37 Mbp region of chromosome 13 previously identified by exclusion mapping was consistently associated with a reduction of salt-induced hypertension in the Dahl salt-sensitive (SS) rat. This region contained five genes that were introgressed from the salt-insensitive Brown Norway (BN) rat. The goal of the present study was to further narrow that region to identify the gene(s) most likely to protect from salt-induced hypertension. The studies yielded a subcongenic SS rat strain containing a 0.71 Mbp insert from BN (26-P strain) in which salt-induced hypertension was reduced by 24 mmHg. The region contained two protein-coding genes ( Astn1 and Pappa2) and a microRNA ( miR-488). Pappa2 mRNA in the renal cortex of the protected 26-P was 6- to 10-fold greater than in SS fed a 0.4% NaCl diet but was reduced to levels observed in SS when fed 8.0% NaCl diet for 7 days. Compared with brain nuclei (NTS, RVLM, CVLM) and the adrenal gland, Pappa2 in the renal cortex was the only gene found to be differentially expressed between SS and 26-P and that responded to changes of salt diet. Immunohistochemistry studies found Pappa2 localized in the cytosol of the epithelial cells of the cortical thick ascending limbs. In more distal segments of the renal tubules, it was observed within tubular lumens and most notably bound to the apical membranes of the intercalated cells of collecting ducts. We conclude that we have identified a variant form of Pappa2 that can protect against salt-induced hypertension in the Dahl S rat.

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14

Cowley, Allen W., Carol Moreno, Howard J. Jacob, Christine B. Peterson, Francesco C. Stingo, Kwang Woo Ahn, Pengyuan Liu, et al. "Characterization of biological pathways associated with a 1.37 Mbp genomic region protective of hypertension in Dahl S rats." Physiological Genomics 46, no. 11 (June 1, 2014): 398–410. http://dx.doi.org/10.1152/physiolgenomics.00179.2013.

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The goal of the present study was to narrow a region of chromosome 13 to only several genes and then apply unbiased statistical approaches to identify molecular networks and biological pathways relevant to blood-pressure salt sensitivity in Dahl salt-sensitive (SS) rats. The analysis of 13 overlapping subcongenic strains identified a 1.37 Mbp region on chromosome 13 that influenced the mean arterial blood pressure by at least 25 mmHg in SS rats fed a high-salt diet. DNA sequencing and analysis filled genomic gaps and provided identification of five genes in this region, Rfwd2, Fam5b, Astn1, Pappa2, and Tnr. A cross-platform normalization of transcriptome data sets obtained from our previously published Affymetrix GeneChip dataset and newly acquired RNA-seq data from renal outer medullary tissue provided 90 observations for each gene. Two Bayesian methods were used to analyze the data: 1) a linear model analysis to assess 243 biological pathways for their likelihood to discriminate blood pressure levels across experimental groups and 2) a Bayesian graphical modeling of pathways to discover genes with potential relationships to the candidate genes in this region. As none of these five genes are known to be involved in hypertension, this unbiased approach has provided useful clues to be experimentally explored. Of these five genes, Rfwd2, the gene most strongly expressed in the renal outer medulla, was notably associated with pathways that can affect blood pressure via renal transcellular Na+ and K+ electrochemical gradients and tubular Na+ transport, mitochondrial TCA cycle and cell energetics, and circadian rhythms.

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15

McLellan, Heather. "ASTNA." Air Medical Journal 22, no. 6 (November 2003): 11–12. http://dx.doi.org/10.1016/j.amj.2003.10.013.

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16

Lystrup, Ann. "ASTNA." Air Medical Journal 23, no. 6 (November 2004): 14–15. http://dx.doi.org/10.1016/j.amj.2004.10.001.

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17

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 1 (January 2005): 14–15. http://dx.doi.org/10.1016/j.amj.2004.11.004.

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18

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 2 (March 2005): 61. http://dx.doi.org/10.1016/j.amj.2005.01.004.

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19

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 3 (May 2005): 103–4. http://dx.doi.org/10.1016/j.amj.2005.03.005.

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20

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 4 (July 2005): 140–41. http://dx.doi.org/10.1016/j.amj.2005.05.005.

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21

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 5 (September 2005): 186–87. http://dx.doi.org/10.1016/j.amj.2005.07.038.

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22

Hignite, Jodie. "ASTNA." Air Medical Journal 24, no. 6 (November 2005): 230. http://dx.doi.org/10.1016/j.amj.2005.09.003.

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23

Mogues, Tirsit, Michael Etzerodt, Crystal Hall, Georg Engelich, Jonas H. Graversen, and Kevan L. Hartshorn. "Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity." Journal of Biomedicine and Biotechnology 2004, no. 2 (2004): 73–78. http://dx.doi.org/10.1155/s1110724304307096.

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Tetranectin is a plasminogen kringle 4 domain-binding protein present in plasma and various tissue locations. Decreased plasma tetranectin or increased tetranectin in stroma of cancers correlates with cancer progression and adverse prognosis. A possible mechanism through which tetranectin could influence cancer progression is by altering activities of plasminogen or the plasminogen fragment, angiostatin. Tetranectin was found to bind to the kringle 1-4 form of angiostatin (ASTK1-4). In addition, tetranectin inhibited binding of plasminogen or ASTK1-4to extracellular matrix (ECM) deposited by endothelial cells. Finally, tetranectin partially counteracted the ability of ASTK1-4to inhibit proliferation of endothelial cells. This latter effect of tetranectin was specific for ASTK1-4since it did not counteract the antiproliferative activities of the kringle 1-3 form of angiostatin (ASTK1-3) or endostatin. These findings suggest that tetranectin may modulate angiogenesis through interactions with AST.

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24

Ni, Tao, Karl Harlos, and Robert Gilbert. "Structure of astrotactin-2: a conserved vertebrate-specific and perforin-like membrane protein involved in neuronal development." Open Biology 6, no. 5 (May 2016): 160053. http://dx.doi.org/10.1098/rsob.160053.

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The vertebrate-specific proteins astrotactin-1 and 2 (ASTN-1 and ASTN-2) are integral membrane perforin-like proteins known to play critical roles in neurodevelopment, while ASTN-2 has been linked to the planar cell polarity pathway in hair cells. Genetic variations associated with them are linked to a variety of neurodevelopmental disorders and other neurological pathologies, including an advanced onset of Alzheimer's disease. Here we present the structure of the majority endosomal region of ASTN-2, showing it to consist of a unique combination of polypeptide folds: a perforin-like domain, a minimal epidermal growth factor-like module, a unique form of fibronectin type III domain and an annexin-like domain. The perforin-like domain differs from that of other members of the membrane attack complex-perforin (MACPF) protein family in ways that suggest ASTN-2 does not form pores. Structural and biophysical data show that ASTN-2 (but not ASTN-1) binds inositol triphosphates, suggesting a mechanism for membrane recognition or secondary messenger regulation of its activity. The annexin-like domain is closest in fold to repeat three of human annexin V and similarly binds calcium, and yet shares no sequence homology with it. Overall, our structure provides the first atomic-resolution description of a MACPF protein involved in development, while highlighting distinctive features of ASTN-2 responsible for its activity.

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25

Burt, Olivia, Keira J. A. Johnston, Nicholas Graham, Breda Cullen, Donald M. Lyall, Laura M. Lyall, Jill P. Pell, Joey Ward, Daniel J. Smith, and Rona J. Strawbridge. "Genetic Variation in the ASTN2 Locus in Cardiovascular, Metabolic and Psychiatric Traits: Evidence for Pleiotropy Rather Than Shared Biology." Genes 12, no. 8 (July 31, 2021): 1194. http://dx.doi.org/10.3390/genes12081194.

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Background: The link between cardiometabolic and psychiatric illness has long been attributed to human behaviour, however recent research highlights shared biological mechanisms. The ASTN2 locus has been previously implicated in psychiatric and cardiometabolic traits, therefore this study aimed to systematically investigate the genetic architecture of ASTN2 in relation to a wide range of relevant traits. Methods: Baseline questionnaire, assessment and genetic data of 402111 unrelated white British ancestry individuals from the UK Biobank was analysed. Genetic association analyses were conducted using PLINK 1.07, assuming an additive genetic model and adjusting for age, sex, genotyping chip, and population structure. Conditional analyses and linkage disequilibrium assessment were used to determine whether cardiometabolic and psychiatric signals were independent. Results: Associations between genetic variants in the ASTN2 locus and blood pressure, total and central obesity, neuroticism, anhedonia and mood instability were identified. All analyses support the independence of the cardiometabolic traits from the psychiatric traits. In silico analyses provide support for the central obesity signal acting through ASTN2, however most of the other signals are likely acting through other genes in the locus. Conclusions: Our systematic analysis demonstrates that ASTN2 has pleiotropic effects on cardiometabolic and psychiatric traits, rather than contributing to shared pathology.

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26

Chang, A., and G. R. Fink. "Targeting of the yeast plasma membrane [H+]ATPase: a novel gene AST1 prevents mislocalization of mutant ATPase to the vacuole." Journal of Cell Biology 128, no. 1 (January 1, 1995): 39–49. http://dx.doi.org/10.1083/jcb.128.1.39.

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We have characterized a class of mutations in PMA1, (encoding plasma membrane ATPase) that is ideal for the analysis of membrane targeting in Saccharomyces cerevisiae. This class of pma1 mutants undergoes growth arrest at the restrictive temperature because newly synthesized ATPase fails to be targeted to the cell surface. Instead, mutant ATPase is delivered to the vacuole, where it is degraded. Delivery to the vacuole occurs without previous arrival at the plasma membrane because degradation of mutant ATPase is not prevented when internalization from the cell surface is blocked. Disruption of PEP4, encoding vacuolar proteinase A, blocks ATPase degradation, but fails to restore growth because the ATPase is still improperly targeted. One of these pma1 mutants was used to select multicopy suppressors that would permit growth at the nonpermissive temperature. A novel gene, AST1, identified by this selection, suppresses several pma1 alleles defective for targeting. The basis for suppression is that multicopy AST1 causes rerouting of mutant ATPase from the vacuole to the cell surface. pma1 mutants deleted for AST1 have a synthetic growth defect at the permissive temperature, providing genetic evidence for interaction between AST1 and PMA1. Ast1 is a cytoplasmic protein that associates with membranes, and is localized to multiple compartments, including the plasma membrane. The identification of AST1 homologues suggests that Ast1 belongs to a novel family of proteins that participates in membrane traffic.

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27

Bernier, N. J., and S. F. Perry. "Angiotensins stimulate catecholamine release from the chromaffin tissue of the rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 1 (July 1, 1997): R49—R57. http://dx.doi.org/10.1152/ajpregu.1997.273.1.r49.

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Immunohistochemical and pharmacological techniques were utilized to investigate the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). Double labeling with [Asp1, Ile5]angiotensin II-fluorescein isothiocyanate (ANG II-FITC) and anti-dopamine beta-hydroxylase revealed specific ANG II binding sites on chromaffin cells. Injection (1 nmol/kg body wt) of either ANG II-FITC, [Asn1, Val5, Asn9]ANG I, [Asp1, Ile5, His9]ANG I, [Asn1, Val5]ANG II, [Asp1, Val5]ANG II, or [Asp1, Ile5]ANG II elicited catecholamine release from in situ perfusion preparations of the head kidney. Catecholamine release elicited by [Asn1, Val5]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose dependent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn1, Val5]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 82% lower in response to injections (1 nmol/kg body wt) of [Asn1, Val5]ANG I [amino acid (AA) positions 1-7] and [Asn1, Val5]ANG I (AA 1-6), respectively. Pretreatment with either losartan (10(-5) M), PD-123319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn1, Val5]ANG II-elicited catecholamine release. Pretreatment with captopril (10(-4) M) significantly reduced [Asn1, Val5, Asn9]ANG I-elicited Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catecholamine release from the chromaffin tissue via specific ANG II binding sites and indicate that the synthesis of ANG II may be either local or systemic.

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28

Guo, Tangjun, Aijun Bao, Yandong Xie, Jianting Qiu, and Haozhe Piao. "Single-Cell Sequencing Analysis Identified ASTN2 as a Migration Biomarker in Adult Glioblastoma." Brain Sciences 12, no. 11 (October 30, 2022): 1472. http://dx.doi.org/10.3390/brainsci12111472.

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Glioblastoma is the most common and aggressive primary central nervous system malignant tumors. With the development of targeted sequencing and proteomic profiling technology, some new tumor types have been established and a series of novel molecular markers have also been identified. The 2021 updated World Health Organization classification of central nervous system tumors first mentioned the classification of adult glioma and pediatric glioma based on the molecular diagnosis. Thus, we used single-cell RNA sequencing analysis to explore the diversity and similarities in the occurrence and development of adult and pediatric types. ASTN2, which primarily encodes astrotactin, has been reported to be dysregulated in various neurodevelopmental disorders. Although some studies have demonstrated that ASTN2 plays an important role in glial-guided neuronal migration, there are no studies about its impact on glioblastoma cell migration. Subsequent single-cell RNA sequencing revealed ASTN2 to be a hub gene of a cell cluster which had a poor effect on clinical prognosis. Eventually, a western blot assay and a wound-healing assay first confirmed that ASTN2 expression in glioblastoma cell lines is higher than that in normal human astrocytes and affects the migration ability of glioblastoma cells, making it a potential therapeutic target.

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29

Luo, Le, Ruyi Qin, Tao Liu, Ming Yu, Tingwen Yang, and Guohua Xu. "OsASN1 Plays a Critical Role in Asparagine-Dependent Rice Development." International Journal of Molecular Sciences 20, no. 1 (December 31, 2018): 130. http://dx.doi.org/10.3390/ijms20010130.

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Asparagine is one of the important amino acids for long-distance transport of nitrogen (N) in plants. However, little is known about the effect of asparagine on plant development, especially in crops. Here, a new T-DNA insertion mutant, asparagine synthetase 1 (asn1), was isolated and showed a different plant height, root length, and tiller number compared with wild type (WT). In asn1, the amount of asparagine decreased sharply while the total nitrogen (N) absorption was not influenced. In later stages, asn1 showed reduced tiller number, which resulted in suppressed tiller bud outgrowth. The relative expression of many genes involved in the asparagine metabolic pathways declined in accordance with the decreased amino acid concentration. The CRISPR/Cas9 mutant lines of OsASN1 showed similar phenotype with asn1. These results suggest that OsASN1 is involved in the regulation of rice development and is specific for tiller outgrowth.

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30

Yang, Ming, Eric T. Kimchi, Kevin F. Staveley-O’Carroll, and Guangfu Li. "Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity." International Journal of Molecular Sciences 22, no. 20 (October 13, 2021): 11037. http://dx.doi.org/10.3390/ijms222011037.

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Dietary change leads to a precipitous increase in non-alcoholic fatty liver disease (NAFLD) from simple steatosis to the advanced form of non-alcoholic steatohepatitis (NASH), affecting approximately 25% of the global population. Although significant efforts greatly advance progress in clarifying the pathogenesis of NAFLD and identifying therapeutic targets, no therapeutic agent has been approved. Astaxanthin (ASTN), a natural antioxidant product, exerts an anti-inflammation and anti-fibrotic effect in mice induced with carbon tetrachloride (CCl4) and bile duct ligation (BDL); thus, we proposed to further investigate the potential effect of ASTN on a diet-induced mouse NASH and liver fibrosis, as well as the underlying cellular and molecular mechanisms. By treating pre-development of NASH in mice induced with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), we have demonstrated that oral administration ASTN preventively ameliorated NASH development and liver fibrosis by modulating the hepatic immune response, liver inflammation, and oxidative stress. Specifically, ASTN treatment led to the reduction in liver infiltration of monocyte-derived macrophages, hepatic stellate cell (HSC) activation, oxidative stress response, and hepatocyte death, accompanied by the decreased hepatic gene expression of proinflammatory cytokines such as TNF-α, TGF-β1, and IL-1β. In vitro studies also demonstrated that ASTN significantly inhibited the expression of proinflammatory cytokines and chemokine CCL2 in macrophages in response to lipopolysaccharide (LPS) stimulation. Overall, in vivo and in vitro studies suggest that ASTN functions as a promising therapeutic agent to suppress NASH and liver fibrosis via modulating intrahepatic immunity.

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31

Yang, Ming, Eric T. Kimchi, Kevin F. Staveley-O’Carroll, and Guangfu Li. "Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity." International Journal of Molecular Sciences 22, no. 20 (October 13, 2021): 11037. http://dx.doi.org/10.3390/ijms222011037.

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Анотація:

Dietary change leads to a precipitous increase in non-alcoholic fatty liver disease (NAFLD) from simple steatosis to the advanced form of non-alcoholic steatohepatitis (NASH), affecting approximately 25% of the global population. Although significant efforts greatly advance progress in clarifying the pathogenesis of NAFLD and identifying therapeutic targets, no therapeutic agent has been approved. Astaxanthin (ASTN), a natural antioxidant product, exerts an anti-inflammation and anti-fibrotic effect in mice induced with carbon tetrachloride (CCl4) and bile duct ligation (BDL); thus, we proposed to further investigate the potential effect of ASTN on a diet-induced mouse NASH and liver fibrosis, as well as the underlying cellular and molecular mechanisms. By treating pre-development of NASH in mice induced with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), we have demonstrated that oral administration ASTN preventively ameliorated NASH development and liver fibrosis by modulating the hepatic immune response, liver inflammation, and oxidative stress. Specifically, ASTN treatment led to the reduction in liver infiltration of monocyte-derived macrophages, hepatic stellate cell (HSC) activation, oxidative stress response, and hepatocyte death, accompanied by the decreased hepatic gene expression of proinflammatory cytokines such as TNF-α, TGF-β1, and IL-1β. In vitro studies also demonstrated that ASTN significantly inhibited the expression of proinflammatory cytokines and chemokine CCL2 in macrophages in response to lipopolysaccharide (LPS) stimulation. Overall, in vivo and in vitro studies suggest that ASTN functions as a promising therapeutic agent to suppress NASH and liver fibrosis via modulating intrahepatic immunity.

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32

Najem Abed, Nisreen Abdul Rahman, Suha Mujahed Abudoleh, Iyad Daoud Alshawabkeh, Abdul Rahman Najem Abed, Rasha Khaled Ali Abuthawabeh, and Samer Hasan Hussein-Al-Ali. "Aspirin Drug Intercalated into Zinc-Layered Hydroxides as Nanolayers: Structure and In Vitro Release." Nano Hybrids and Composites 18 (November 2017): 42–52. http://dx.doi.org/10.4028/www.scientific.net/nhc.18.42.

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Zinc layered hydroxides (ZLHs) can be used as host materials for drug-ZLH host–guest structures. Aspirin with 0.1 and 0.4 M were intercalated into zinc layered hydroxides to form aspirin nanocomposites; ASPN1 and ASPN4, respectively. From XRD and software, the interlayer spacing of ASPN1 and ASPN4 was 15.2 Å. The result coupled with molecular geometry calculation indicates that the spatial orientation of the drug in the ZLH was monolayer for ASPN1 and ASPN4 nanocomposites. The release of the aspirin from ASPN4 nanocomposite at pH 6.8 is 35%, compared to 98% at pH 1.2, and followed Hixson model and Korsmeyer model for ASPN4 at pH 6.8 and pH 1.2, respectively. This result indicates sustained release of the drugs from their respective nanocomposites, and therefore these nanocomposites have good potential to be used as controlled-release formulation of the aspirin. The ASPN4 nanocomposite was highly effective to Escherichia coli compared to free aspirin, where the ASPN4 given 1.37 inhibition zone compared to aspirin which given 1.17 cm inhibition zone.

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33

Williams, Ken, Jill Johnson, Gary L. Campbell, and Christian R. Giller. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 20, no. 6 (December 2001): 0037–40. http://dx.doi.org/10.1067/mmj.2001.120091.

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34

Giller, Christian, G. Powell, Ken Williams, Jill Johnson, and Victoria A. Spediacci. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 21, no. 2 (April 2002): 14–16. http://dx.doi.org/10.1067/mmj.2002.122911.

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35

Powell, Greg, Ken Williams, Jill Johnson, and Christian Giller. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 21, no. 3 (June 2002): 14–30. http://dx.doi.org/10.1067/mmj.2002.124228.

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36

Williams, Ken, Jill Johnson, Gary L. Campbell, and Thomas P. Judge. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 21, no. 4 (August 2002): 12–14. http://dx.doi.org/10.1067/mmj.2002.125943.

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37

Johnson, Jill, Christian Giller, D. Gregory Powell, and Ken Williams. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 21, no. 5 (October 2002): 13–15. http://dx.doi.org/10.1067/mmj.2002.127617.

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38

Chesney, Michael L. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 21, no. 6 (December 2002): 15–17. http://dx.doi.org/10.1067/mmj.2002.129355.

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39

Huss, Brian. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 22, no. 2 (April 2003): 14–15. http://dx.doi.org/10.1067/mmj.2003.31.

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40

Bradin, Stuart A. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 22, no. 3 (June 2003): 12–13. http://dx.doi.org/10.1067/mmj.2003.44.

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41

Frazer, Eileen. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 22, no. 4 (August 2003): 10–11. http://dx.doi.org/10.1067/mmj.2003.61.

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42

Kennedy, TJ, D. Gregory Powell, Harry Sibold, Heather McLellan, and Gary L. Campbell. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." AirMed 22, no. 1 (February 2003): 10–13. http://dx.doi.org/10.1067/mmj.2003.mmj0316.

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43

Williams, Ken, Jill Johnson, Gary L. Campbell, and Christian R. Giller. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 20, no. 6 (November 2001): 37–40. http://dx.doi.org/10.1016/s1067-991x(01)70018-1.

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44

Johnson, Jill, Christian Giller, D. Gregory Powell, and Ken Williams. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 21, no. 5 (September 2002): 13–15. http://dx.doi.org/10.1016/s1067-991x(02)70012-6.

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45

Powell, Greg, Ken Williams, Jill Johnson, and Christian Giller. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 21, no. 3 (May 2002): 14–16. http://dx.doi.org/10.1016/s1067-991x(02)70045-x.

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46

Williams, Ken, Jill Johnson, Gary L. Campbell, and Thomas P. Judge. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 21, no. 4 (July 2002): 12–14. http://dx.doi.org/10.1016/s1067-991x(02)70063-1.

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47

Giller, Christian, G. Powell, Ken Williams, Jill Johnson, and Victoria A. Spediacci. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 21, no. 2 (March 2002): 14–16. http://dx.doi.org/10.1016/s1067-991x(02)70092-8.

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48

Johnson, Jill. "ASTNA Critical care transport nurses day." Air Medical Journal 21, no. 1 (January 2002): 35. http://dx.doi.org/10.1016/s1067-991x(02)80035-9.

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49

Kennedy, TJ, D. Gregory Powell, Harry Sibold, Heather McLellan, and Gary L. Campbell. "Forum: AAMS, AMPA, ASTNA, NEMSPA, NFPA." Air Medical Journal 22, no. 1 (January 2003): 10–13. http://dx.doi.org/10.1016/s1067-991x(03)70030-3.

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50

He, Yizhou Joseph, and Dipanjan Chowdhury. "ASTE1 cutting to block DNA end resection." Nature Cell Biology 23, no. 8 (August 2021): 818–19. http://dx.doi.org/10.1038/s41556-021-00731-9.

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