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Article ; Online: Effect of Resin Content on the Structure, Water Resistance and Mechanical Properties of High-Density Bamboo Scrimbers.

Yang, Zixuan / Meng, Xin / Zeng, Guangda / Wei, Jinguang / Wang, Chuangui / Yu, Wenji

2024 Volume 16, Issue 6

Abstract: Bamboo scrimber is acknowledged for its eco-friendly potential as a structural material. Its properties are significantly affected by both its density and resin content, but the effect of resin content on the properties under high density is not yet ... ...

Abstract	Bamboo scrimber is acknowledged for its eco-friendly potential as a structural material. Its properties are significantly affected by both its density and resin content, but the effect of resin content on the properties under high density is not yet known. In this study, the microstructure, water resistance, mechanical properties, and thermal stability of bamboo scrimbers with varying resin content at a density of 1.30 g/cm
Language	English
Publishing date	2024-03-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527146-5
ISSN	2073-4360 ; 2073-4360
ISSN (online)	2073-4360
ISSN	2073-4360
DOI	10.3390/polym16060797
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A New Type of Nanocomposite Based on Bamboo Parenchymal Cells

Shuangyan, Zhang / Wang Chuangui

Forest products journal. 2017, v. 67, no. 3-4

2017

Abstract: In this study, a kind of nanocomposite was prepared using nanocellulose fibril (NCF) aerogels derived from processed bamboo residues composed mainly of parenchymal cells. NCF aerogels were prepared using an ultrasonication method with freeze-drying. The ... ...

Abstract	In this study, a kind of nanocomposite was prepared using nanocellulose fibril (NCF) aerogels derived from processed bamboo residues composed mainly of parenchymal cells. NCF aerogels were prepared using an ultrasonication method with freeze-drying. The freeze-dried aerogels were swollen with water and then impregnated with aqueous phenol-formaldehyde resin solutions of varying concentrations. The mechanical properties of nanocomposites with 10 percent (by weight) resin exhibited a tensile strength, tensile modulus, and tensile toughness of 150 MPa, 5 GPa, and 17 MJ/m3, respectively. Compared with NCF aerogels, the composites demonstrated lower hygroscopicity at high humidity. This combination of toughness, minimal moisture absorption, and other properties is of technical interest for practical applications.
Keywords	absorption ; aerogels ; bamboos ; cellulose ; freeze drying ; humidity ; hygroscopicity ; nanocomposites ; tensile strength ; ultrasonic treatment
Language	English
Size	p. 283-287.
Publishing place	[Forest Products Society, etc.]
Document type	Article
ZDB-ID	240509-x
ISSN	0015-7473
ISSN	0015-7473
DOI	10.13073/FPJ-D-16-00043
Database	NAL-Catalogue (AGRICOLA)

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Article: Biological Degradation of Chinese Fir with Trametes Versicolor (L.) Lloyd.

Chen, Meiling / Wang, Chuangui / Fei, Benhua / Ma, Xinxin / Zhang, Bo / Zhang, Shuangyan / Huang, Anmin

Materials (Basel, Switzerland)

2017 Volume 10, Issue 7

Abstract: Chinese fir ( ...

Abstract	Chinese fir (
Language	English
Publishing date	2017-07-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2487261-1
ISSN	1996-1944
ISSN	1996-1944
DOI	10.3390/ma10070834
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The ATM and ATR kinases regulate centrosome clustering and tumor recurrence by targeting KIFC1 phosphorylation.

Fan, Guangjian / Sun, Lianhui / Meng, Ling / Hu, Chen / Wang, Xing / Shi, Zhan / Hu, Congli / Han, Yang / Yang, Qingqing / Cao, Liu / Zhang, Xiaohong / Zhang, Yan / Song, Xianmin / Xia, Shujie / He, Baokun / Zhang, Shengping / Wang, Chuangui

Nature communications

2021 Volume 12, Issue 1, Page(s) 20

Abstract: Drug resistance and tumor recurrence are major challenges in cancer treatment. Cancer cells often display centrosome amplification. To maintain survival, cancer cells achieve bipolar division by clustering supernumerary centrosomes. Targeting centrosome ... ...

Abstract	Drug resistance and tumor recurrence are major challenges in cancer treatment. Cancer cells often display centrosome amplification. To maintain survival, cancer cells achieve bipolar division by clustering supernumerary centrosomes. Targeting centrosome clustering is therefore considered a promising therapeutic strategy. However, the regulatory mechanisms of centrosome clustering remain unclear. Here we report that KIFC1, a centrosome clustering regulator, is positively associated with tumor recurrence. Under DNA damaging treatments, the ATM and ATR kinases phosphorylate KIFC1 at Ser26 to selectively maintain the survival of cancer cells with amplified centrosomes via centrosome clustering, leading to drug resistance and tumor recurrence. Inhibition of KIFC1 phosphorylation represses centrosome clustering and tumor recurrence. This study identified KIFC1 as a prognostic tumor recurrence marker, and revealed that tumors can acquire therapeutic resistance and recurrence via triggering centrosome clustering under DNA damage stresses, suggesting that blocking KIFC1 phosphorylation may open a new vista for cancer therapy.
MeSH term(s)	Amino Acid Sequence ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Cell Line, Tumor ; Centrosome/metabolism ; Chromosomal Instability ; DNA Damage ; Drug Resistance, Neoplasm ; Humans ; Kinesin/chemistry ; Kinesin/metabolism ; Mice ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Phosphorylation ; Phosphoserine/metabolism
Chemical Substances	KIFC1 protein, human ; Phosphoserine (17885-08-4) ; ATM protein, human (EC 2.7.11.1) ; ATR protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2021-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-20208-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Inhibition of SIRT2 promotes APP acetylation and ameliorates cognitive impairment in APP/PS1 transgenic mice.

Bai, Ning / Li, Na / Cheng, Rong / Guan, Yi / Zhao, Xiong / Song, Zhijie / Xu, Hongde / Yi, Fei / Jiang, Bo / Li, Xiaoman / Wu, Xuan / Jiang, Cui / Zhou, Tingting / Guo, Qiqiang / Guo, Wendong / Feng, Yanling / Wang, Zhuo / Ma, Mengtao / Yu, Yang /

Wang, Zhanyou / Zhang, Shengping / Wang, Chuangui / Zhao, Weidong / Liu, Shihui / Song, Xiaoyu / Liu, Hua / Cao, Liu

Cell reports

2022 Volume 40, Issue 2, Page(s) 111062

Abstract: Aging is a primary risk factor for neurodegenerative diseases, such as Alzheimer's disease (AD). SIRT2, an ... ...

Abstract	Aging is a primary risk factor for neurodegenerative diseases, such as Alzheimer's disease (AD). SIRT2, an NAD
MeSH term(s)	Acetylation ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Cognitive Dysfunction ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Presenilin-1/metabolism ; Protein Processing, Post-Translational ; Sirtuin 2/genetics ; Sirtuin 2/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Presenilin-1 ; Sirtuin 2 (EC 3.5.1.-)
Language	English
Publishing date	2022-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111062
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: FOXQ1 recruits the MLL complex to activate transcription of EMT and promote breast cancer metastasis.

Nature communications

2022 Volume 13, Issue 1, Page(s) 6548

Abstract: Aberrant expression of the Forkhead box transcription factor, FOXQ1, is a prevalent mechanism of epithelial-mesenchymal transition (EMT) and metastasis in multiple carcinoma types. However, it remains unknown how FOXQ1 regulates gene expression. Here, we ...

Abstract	Aberrant expression of the Forkhead box transcription factor, FOXQ1, is a prevalent mechanism of epithelial-mesenchymal transition (EMT) and metastasis in multiple carcinoma types. However, it remains unknown how FOXQ1 regulates gene expression. Here, we report that FOXQ1 initiates EMT by recruiting the MLL/KMT2 histone methyltransferase complex as a transcriptional coactivator. We first establish that FOXQ1 promoter recognition precedes MLL complex assembly and histone-3 lysine-4 trimethylation within the promoter regions of critical genes in the EMT program. Mechanistically, we identify that the Forkhead box in FOXQ1 functions as a transactivation domain directly binding the MLL core complex subunit RbBP5 without interrupting FOXQ1 DNA binding activity. Moreover, genetic disruption of the FOXQ1-RbBP5 interaction or pharmacologic targeting of KMT2/MLL recruitment inhibits FOXQ1-dependent gene expression, EMT, and in vivo tumor progression. Our study suggests that targeting the FOXQ1-MLL epigenetic axis could be a promising strategy to combat triple-negative breast cancer metastatic progression.
MeSH term(s)	Female ; Humans ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition/physiology ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation, Neoplastic ; Neoplasms, Second Primary/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Melanoma, Cutaneous Malignant
Chemical Substances	Forkhead Transcription Factors ; FOXQ1 protein, human ; Myeloid-Lymphoid Leukemia Protein (149025-06-9)
Language	English
Publishing date	2022-11-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-34239-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: METTL3 acetylation impedes cancer metastasis via fine-tuning its nuclear and cytosolic functions.

Li, Yuanpei / He, Xiaoniu / Lu, Xiao / Gong, Zhicheng / Li, Qing / Zhang, Lei / Yang, Ronghui / Wu, Chengyi / Huang, Jialiang / Ding, Jiancheng / He, Yaohui / Liu, Wen / Chen, Ceshi / Cao, Bin / Zhou, Dawang / Shi, Yufeng / Chen, Juxiang / Wang, Chuangui / Zhang, Shengping /

Zhang, Jian / Ye, Jing / You, Han

Nature communications

2022 Volume 13, Issue 1, Page(s) 6350

Abstract: The methyltransferase like 3 (METTL3) has been generally recognized as a nuclear protein bearing oncogenic properties. We find predominantly cytoplasmic METTL3 expression inversely correlates with node metastasis in human cancers. It remains unclear if ... ...

Abstract	The methyltransferase like 3 (METTL3) has been generally recognized as a nuclear protein bearing oncogenic properties. We find predominantly cytoplasmic METTL3 expression inversely correlates with node metastasis in human cancers. It remains unclear if nuclear METTL3 is functionally distinct from cytosolic METTL3 in driving tumorigenesis and, if any, how tumor cells sense oncogenic insults to coordinate METTL3 functions within these intracellular compartments. Here, we report an acetylation-dependent regulation of METTL3 localization that impacts on metastatic dissemination. We identify an IL-6-dependent positive feedback axis to facilitate nuclear METTL3 functions, eliciting breast cancer metastasis. IL-6, whose mRNA transcript is subjected to METTL3-mediated m
MeSH term(s)	Humans ; Female ; Methyltransferases/metabolism ; Acetylation ; Sirtuin 1/metabolism ; Interleukin-6/metabolism ; RNA, Messenger/metabolism ; Carcinogenesis ; Breast Neoplasms/genetics ; Nuclear Proteins/metabolism ; Aspirin
Chemical Substances	Methyltransferases (EC 2.1.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Interleukin-6 ; RNA, Messenger ; Nuclear Proteins ; Aspirin (R16CO5Y76E) ; METTL3 protein, human (EC 2.1.1.62)
Language	English
Publishing date	2022-10-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-34209-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The USP10-HDAC6 axis confers cisplatin resistance in non-small cell lung cancer lacking wild-type p53.

Hu, Chen / Zhang, Mu / Moses, Niko / Hu, Cong-Li / Polin, Lisa / Chen, Wei / Jang, Hyejeong / Heyza, Joshua / Malysa, Agnes / Caruso, Joseph A / Xiang, Shengyan / Patrick, Steve / Stemmer, Paul / Lou, Zhenkun / Bai, Wenlong / Wang, Chuangui / Bepler, Gerold / Zhang, Xiaohong Mary

Cell death & disease

2020 Volume 11, Issue 5, Page(s) 328

Abstract: Ubiquitin-specific peptidase 10 (USP10) stabilizes both tumor suppressors and oncogenes in a context-dependent manner. However, the nature of USP10's role in non-small cell lung cancer (NSCLC) remains unclear. By analyzing The Cancer Genome Atlas (TCGA) ... ...

Abstract	Ubiquitin-specific peptidase 10 (USP10) stabilizes both tumor suppressors and oncogenes in a context-dependent manner. However, the nature of USP10's role in non-small cell lung cancer (NSCLC) remains unclear. By analyzing The Cancer Genome Atlas (TCGA) database, we have shown that high levels of USP10 are associated with poor overall survival in NSCLC with mutant p53, but not with wild-type p53. Consistently, genetic depletion or pharmacological inhibition of USP10 dramatically reduces the growth of lung cancer xenografts lacking wild-type p53 and sensitizes them to cisplatin. Mechanistically, USP10 interacts with, deubiquitinates, and stabilizes oncogenic protein histone deacetylase 6 (HDAC6). Furthermore, reintroducing either USP10 or HDAC6 into a USP10-knockdown NSCLC H1299 cell line with null-p53 renders cisplatin resistance. This result suggests the existence of a "USP10-HDAC6-cisplatin resistance" axis. Clinically, we have found a positive correlation between USP10 and HDAC6 expression in a cohort of NSCLC patient samples. Moreover, we have shown that high levels of USP10 mRNA correlate with poor overall survival in a cohort of advanced NSCLC patients who received platinum-based chemotherapy. Overall, our studies suggest that USP10 could be a potential biomarker for predicting patient response to platinum, and that targeting USP10 could sensitize lung cancer patients lacking wild-type p53 to platinum-based therapy.
MeSH term(s)	Animals ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Line, Tumor ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Knockdown Techniques ; Histone Deacetylase 6/metabolism ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice, SCID ; Mutation/genetics ; Ovarian Neoplasms/pathology ; Platinum/pharmacology ; Protein Binding/drug effects ; Protein Stability/drug effects ; Signal Transduction/drug effects ; Substrate Specificity/drug effects ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/metabolism ; Ubiquitin Thiolesterase/metabolism ; Ubiquitination/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Tumor Suppressor Protein p53 ; USP10 protein, human ; Platinum (49DFR088MY) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Histone Deacetylase 6 (EC 3.5.1.98) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-05-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-2519-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Phosphorylation and hsp90 binding mediate heat shock stabilization of p53.

Wang, Chuangui / Chen, Jiandong

The Journal of biological chemistry

2002 Volume 278, Issue 3, Page(s) 2066–2071

Abstract: The p53 tumor suppressor is stabilized and activated by diverse stress signals. In this study, we investigated the mechanism of p53 activation by heat shock. We found that heat shock inhibited p53 ubiquitination and caused accumulation of p53 at the post- ...

Abstract	The p53 tumor suppressor is stabilized and activated by diverse stress signals. In this study, we investigated the mechanism of p53 activation by heat shock. We found that heat shock inhibited p53 ubiquitination and caused accumulation of p53 at the post-transcriptional level. Heat shock induced phosphorylation of p53 at serine 15 in an ATM kinase-dependent fashion, which may contribute partially to heat-induced p53 accumulation. However, p53 accumulation also occurred after heat shock in ATM-deficient cells. Heat shock induced conformational change of wild type p53 and binding to hsp90. Inhibition of hsp90-p53 interaction by geldanamycin prevented p53 accumulation partially in ATM-wild type cells and completely in ATM-deficient cells. Therefore, phosphorylation and interaction with hsp90 both contribute to stabilization of p53 after heat shock.
MeSH term(s)	HSP90 Heat-Shock Proteins/metabolism ; Heat-Shock Response ; Humans ; Phosphorylation ; Protein Binding ; Protein Conformation ; Serine/chemistry ; Serine/metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	HSP90 Heat-Shock Proteins ; Tumor Suppressor Protein p53 ; Serine (452VLY9402)
Language	English
Publishing date	2002-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M206697200
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: HMGB1 released by irradiated tumor cells promotes living tumor cell proliferation via paracrine effect.

He, Sijia / Cheng, Jin / Sun, Lianhui / Wang, Yiwei / Wang, Chuangui / Liu, Xinjian / Zhang, Zhengxiang / Zhao, Minghui / Luo, Yuntao / Tian, Ling / Li, Chuanyuan / Huang, Qian

Cell death & disease

2018 Volume 9, Issue 6, Page(s) 648

Abstract: Tumor repopulation during therapy is an important cause of treatment failure. Strategies to overcome repopulation are arising in parallel with advances in the comprehension of underlying biological mechanisms. Here, we reveal a new mechanism by which ... ...

Abstract	Tumor repopulation during therapy is an important cause of treatment failure. Strategies to overcome repopulation are arising in parallel with advances in the comprehension of underlying biological mechanisms. Here, we reveal a new mechanism by which high mobility group box 1 (HMGB1) released by dying cells during radiotherapy or chemotherapy could stimulate living tumor cell proliferationInhibition or genetic ablation of HMGB1 suppressed tumor cell proliferation. This effect was due to binding of HMGB1with the member receptor for advanced glycation end-products (RAGE), which activated downstream ERK and p38 signaling pathway and promoted cell proliferation. Furthermore, higher HMGB1 expression in tumor tissue correlated with poor overall survival and higher HMGB1 concentration was detected in serum of patients who accepted radiotherapy. Collectively, the results from this study suggested that interaction between dead cells and surviving cells might influence the fate of tumor. HMGB1 could be a novel tumor promoter with therapeutic and prognostic relevance in cancers.
MeSH term(s)	Antigens, Neoplasm/metabolism ; Cell Line, Tumor ; Cell Proliferation/radiation effects ; Cell Survival/radiation effects ; Female ; HMGB1 Protein/metabolism ; Humans ; MAP Kinase Signaling System/radiation effects ; Male ; Middle Aged ; Mitogen-Activated Protein Kinases/metabolism ; Multivariate Analysis ; Neoplasms/metabolism ; Neoplasms/pathology ; Paracrine Communication/radiation effects ; Prognosis ; Protein Binding ; Survival Analysis
Chemical Substances	Antigens, Neoplasm ; HMGB1 Protein ; MOK protein, human (EC 2.7.11.22) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2018-05-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-0626-6
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