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Journal articles

Academic literature on the topic 'Hcinap'

Author: Grafiati

Published: 23 September 2022

Last updated: 28 January 2023

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Journal articles on the topic "Hcinap"

1

Ke, Yanguo, Farhat Abbas, Yiwei Zhou, et al. "Genome-Wide Analysis and Characterization of the Aux/IAA Family Genes Related to Floral Scent Formation in Hedychium coronarium." International Journal of Molecular Sciences 20, no. 13 (2019): 3235. http://dx.doi.org/10.3390/ijms20133235.

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Auxin plays a key role in different plant growth and development processes, including flower opening and development. The perception and signaling of auxin depend on the cooperative action of various components, among which auxin/indole-3-acetic acid (Aux/IAA) proteins play an imperative role. In a recent study, the entire Aux/IAA gene family was identified and comprehensively analyzed in Hedychium coronarium, a scented species used as an ornamental plant for cut flowers. Phylogenetic analysis showed that the Aux/IAA gene family in H. coronarium is slightly contracted compared to Arabidopsis, with low levels of non-canonical proteins. Sequence analysis of promoters showed numerous cis-regulatory elements related to various phytohormones. HcIAA genes showed distinct expression patterns in different tissues and flower developmental stages, and some HcIAA genes showed significant responses to auxin and ethylene, indicating that Aux/IAAs may play an important role in linking hormone signaling pathways. Based on the expression profiles, HcIAA2, HcIAA4, HcIAA6 and HcIAA12, were selected as candidate genes and HcIAA2 and HcIAA4 were screened for further characterization. Downregulation of HcIAA2 and HcIAA4 by virus-induced gene silencing in H. coronarium flowers modified the total volatile compound content, suggesting that HcIAA2 and HcIAA4 play important roles in H. coronarium floral scent formation. The results presented here will provide insights into the putative roles of HcIAA genes and will assist the elucidation of their precise roles during floral scent formation.

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2

Santama, Niovi, Stephen C. Ogg, Anna Malekkou, Spyros E. Zographos, Karsten Weis, and Angus I. Lamond. "Characterization of hCINAP, a Novel Coilin-interacting Protein Encoded by a Transcript from the Transcription Factor TAFIID32 Locus." Journal of Biological Chemistry 280, no. 43 (2005): 36429–41. http://dx.doi.org/10.1074/jbc.m501982200.

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Coilin is a marker protein for the Cajal body, a subnuclear domain acting as a site for assembly and maturation of nuclear RNA-protein complexes. Using a yeast two-hybrid screen to identify coilin-interacting proteins, we have identified hCINAP (human coilin interacting nuclear ATPase protein), a nuclear factor of 172 amino acids with a P-loop nucleotide binding motif and ATPase activity. The hCINAP protein sequence is highly conserved across its full-length from human to plants and yeast and is ubiquitously expressed in all human tissues and cell lines tested. The yeast orthologue of CINAP is a single copy, essential gene. Tagged hCINAP is present in complexes containing coilin in mammalian cells and recombinant, Escherichia coli expressed hCINAP binds directly to coilin in vitro. The 214 carboxyl-terminal residues of coilin appear essential for the interaction with hCINAP. Both immunofluorescence and fluorescent protein tagging show that hCINAP is specifically nuclear and distributed in a widespread, diffuse nucleoplasmic pattern, excluding nucleoli, with some concentration also in Cajal bodies. Overexpression of hCINAP in HeLa cells results in a decrease in the average number of Cajal bodies per nucleus, consistent with it affecting either the stability of Cajal bodies and/or their rate of assembly. The hCINAP mRNA is an alternatively spliced transcript from the TAF9 locus, which encodes the basal transcription factor subunit TAFIID32. However, hCINAP and TAFIID32 mRNAs are translated from different ATG codons and use distinct reading frames, resulting in them having no identity in their respective protein sequences.

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3

Qu, Linglong, Yapeng Ji, Xi Zhu та Xiaofeng Zheng. "hCINAP negatively regulates NF-κB signaling by recruiting the phosphatase PP1 to deactivate IKK complex". Journal of Molecular Cell Biology 7, № 6 (2015): 529–42. http://dx.doi.org/10.1093/jmcb/mjv041.

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4

Malekkou, Anna, Carsten W. Lederer, Angus I. Lamond, and Niovi Santama. "The nuclear ATPase/adenylate kinase hCINAP is recruited to perinucleolar caps generated upon RNA pol.II inhibition." FEBS Letters 584, no. 22 (2010): 4559–64. http://dx.doi.org/10.1016/j.febslet.2010.10.044.

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5

Drakou, Christina E., Anna Malekkou, Joseph M. Hayes, et al. "hCINAP is an atypical mammalian nuclear adenylate kinase with an ATPase motif: Structural and functional studies." Proteins: Structure, Function, and Bioinformatics 80, no. 1 (2011): 206–20. http://dx.doi.org/10.1002/prot.23186.

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6

Zhang, Jinfang, Feiyun Zhang, and Xiaofeng Zheng. "Depletion of hCINAP by RNA interference causes defects in Cajal body formation, histone transcription, and cell viability." Cellular and Molecular Life Sciences 67, no. 11 (2010): 1907–18. http://dx.doi.org/10.1007/s00018-010-0301-2.

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7

Xu, Ruidan, Yongfeng Yang, and Xiaofeng Zheng. "Unique structural features of the adenylate kinase hCINAP/AK6 and its multifaceted functions in carcinogenesis and tumor progression." FEBS Letters 595, no. 16 (2021): 2071–84. http://dx.doi.org/10.1002/1873-3468.14158.

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8

Zhang, J., D. Bai, X. Ma, J. Guan, and X. Zheng. "hCINAP is a novel regulator of ribosomal protein-HDM2-p53 pathway by controlling NEDDylation of ribosomal protein S14." Oncogene 33, no. 2 (2012): 246–54. http://dx.doi.org/10.1038/onc.2012.560.

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9

Zhuge, Ruipeng, Chao Wang, Jie Wang, Shuyu Yu, Liming Liao, and Xiaofeng Zheng. "hCINAP regulates the differentiation of embryonic stem cells by regulating NEDD4 liquid-liquid phase-separation-mediated YAP1 activation." Cell Reports 42, no. 1 (2023): 111935. http://dx.doi.org/10.1016/j.celrep.2022.111935.

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10

St-Arnaud, René, Alice Arabian, Dila Kavame, Martin Kaufmann, and Glenville Jones. "Vitamin D and Diseases of Mineral Homeostasis: A Cyp24a1 R396W Humanized Preclinical Model of Infantile Hypercalcemia Type 1." Nutrients 14, no. 15 (2022): 3221. http://dx.doi.org/10.3390/nu14153221.

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Infantile hypercalcemia type 1 (HCINF1), previously known as idiopathic infantile hypercalcemia, is caused by mutations in the 25-hydroxyvitamin D 24-hydroxylase gene, CYP24A1. The R396W loss-of-function mutation in CYP24A1 is the second most frequent mutated allele observed in affected HCINF1 patients. We have introduced the site-specific R396W mutation within the murine Cyp24a1 gene in knock-in mice to generate a humanized model of HCINF1. On the C57Bl6 inbred background, homozygous mutant mice exhibited high perinatal lethality with 17% survival past weaning. This was corrected by crossbreeding to the CD1 outbred background. Mutant animals had hypercalcemia in the first week of life, developed nephrolithiasis, and had a very high 25(OH)D3 to 24,25(OH)2D3 ratio which is a diagnostic hallmark of the HCINF1 condition. Expression of the mutant Cyp24a1 allele was highly elevated while Cyp27b1 expression was abrogated. Impaired bone fracture healing was detected in CD1-R396w/w mutant animals. The augmented lethality of the C57Bl6-R396W strain suggests an influence of distinct genetic backgrounds. Our data point to the utility of unique knock-in mice to probe the physiological ramifications of CYP24A1 variants in isolation from other biological and environmental factors.

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