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1.
PAPER CURRENT
Evaluation of the toxic effects of celecoxib on Xenopus embryo development (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Yeon-Hee Yoon, Ji Yoon Kim, Yong Chul Bae, Sung-Wook Nam, Hee-Jung Cho, Suho Lee, Ho Young Chung, Hyun-Shik Lee, Mae-Ja Park Celecoxib is a non-steroidal anti-inflammatory drug that selectively inhibits cyclooxygenase-2 and is prescribed for severe pain and inflammation. The excellent therapeutic effects of celecoxib mean that it is frequently used clinically, including for women of child-bearing age. However, the prenatal effects of this compound have not been studied extensively in vertebrates. The present study examined the developmental toxicity of celecoxib using a frog embryo teratogenic assay- Xenopus (FETAX). In addition, we examined its effects on cell migration using co-cultures of human umbilical vein endothelial cells and 10T1/2 cells. These studies revealed that celecoxib induced concentration-dependent mortality and various malformations of the Xenopus internal organs, including gut miscoiling, haemorrhage, and oedema. Celecoxib also downregulated the expression of vascular wall markers (Msr and alpha smooth muscle actin) and other organ-specific markers (Nkx2.5, Cyl104 and IFABP). In vitro co-culture studies revealed that celecoxib inhibited pericyte migration and differentiation into vascular smooth muscle cells. In conclusion, celecoxib was both toxic and teratogenic in Xenopus embryos, where it produced serious heart and vessel malformation by inhibiting vascular wall maturation and vascular network formation.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
2.
PAPER CURRENT
Novel phosphorelay-dependent control of ZFP36L1 protein during the cell cycle (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Makoto Kondo, Aya Noguchi, Yuki Matsuura, Masumi Shimada, Naoto Yokota, Hiroyuki Kawahara The ZFP36 family is a prototypical member of a highly conserved group of proteins with CCCH-type RNA-binding domains, whose functional role and regulatory mechanism in mitotic cells remain obscure. In this study, we provide the first evidence that ZFP36L1 phosphorylation is modulated in a cell cycle-dependent manner. The C-terminal region of ZFP36L1 is critical for its cell cycle-dependent phosphorylation of this protein. We also suggest that the phosphorelay-dependent regulation of ZFP36L1 influences mitotic spindle organization. Thus, our data demonstrate a new class of regulatory mechanism for CCCH-type zinc-finger proteins in cell cycle control.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
3.
PAPER CURRENT
Loss of P53 regresses cardiac remodeling induced by pressure overload partially through inhibiting HIF1α signaling in mice (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Jiming Li, Jingjing Zeng, Lianpin Wu, Luyuan Tao, Zhiyong Liao, Maoping Chu, Lei Li The tumor suppressor p53 is recognized as the guardian of the genome in cell cycle and cell death. P53 expression increases as cardiac hypertrophy worsens to heart failure, suggesting that p53 may play important role in cardiac remodeling. In the present study, deletion of p53 in the mice heart would ameliorate cardiac hypertrophy induced by pressure overload. The role of p53 on heart was investigated using in vivo models. Cardiac hypertrophy in mice was induced by transverse aortic banding surgery. The extent of cardiac hypertrophy was examined by echocardiography, as well as pathological and molecular analyses of heart tissue. Global knockout of p53 in the mice reduced the hypertrophic response and markedly reduced cardiac apoptosis, and fibrosis. Ejection fraction of heart was also improved in hearts without p53 in response to pressure overload. Protein determination further suggested loss of p53 expression markedly increased Hypoxia-inducible factor 1-alpha (HIF1α) and vascular endothelial growth factor (VEGF) expression. The study indicated p53 deteriorated cardiac functions and cardiac hypertrophy, apoptosis, and fibrosis by partially inhibition of HIF1α and VEGF.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
4.
PAPER CURRENT
Structural insight into the role of VAL1 B3 domain for targeting to FLC locus in Arabidopsis thaliana (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Baixing Wu, Mengmeng Zhang, Shichen Su, Hehua Liu, Jianhua Gan, Jinbiao Ma Vernalization is a pivotal stage for some plants involving many epigenetic changes during cold exposure. In Arabidopsis , an essential step in vernalization for further flowering is successful silence the potent floral repressor Flowering Locus C (FLC) by repressing histone mark. At Val1 is a multi-function protein containing five domains that participate into many recognition processes and is validated to recruit the repress histone modifier PHD-PRC2 complex and interact with components of the ASAP complex target to the FLC nucleation region through recognizing a cis element known as CME (cold memory element) by its plant-specific B3 domain. Here, we determine the crystal structure of the B3 domain in complex with Sph/RY motif in CME. Our structural analysis reveals the specific DNA recognition by B3 domain, combined with our in vitro experiments, we provide the structural insight into the important implication of At VAL1-B3 domain in flowering process.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
5.
PAPER CURRENT
CRL4BRBBP7 targets HUWE1 for ubiquitination and proteasomal degradation (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Fei Liu, Li Cao, Ting Zhang, Fen Chang, Yongjie Xu, Qin Li, Jingcheng Deng, Li Li, Genze Shao The E3 ubiquitin ligase HUWE1/Mule/ARF-BP1 plays an important role in diverse biological processes including DNA damage repair and apoptosis. Our previous study has shown that in response to DNA damage HUWE1 was downregulated in CUL4B-mediated ubiquitination and subsequent proteasomal degradation, and CUL4B-mediated regulation of HUWE1 was important for cell survival upon DNA damage. CUL4B is a core component of the CUL4B Ring ligase complexes containing ROC1, DDB1 and a DDB1-Cullin Associated Factors (DCAFs), the latter of which are DDB1-binding WD40 adaptors critical for substrate recognition and recruitment. However, the identity of DCAF in CRL4B that mediates degradation of HUWE1 remains elusive. Here we report that RBBP7 is the DCAF in the CRL4B complex bridging the DDB1-CUL4B-ROC1 to HUWE1. Loading of HUWE1 to the E3 ubiquitin ligase complex resulted in its polyubiquitination, and consequently its proteasome mediated degradation. Overexpression of RBBP7 promoted HUWE1 protein degradation, while depletion of RBBP7 stabilized HUWE1, and hence accelerated the degradation of MCL-1 and BRCA1, two substrates of HUWE1 that are critical in apoptosis and DNA damage repair. Taken together, these data reveal CRL4B RBBP7 is the E3 ligase responsible for the proteasomal degradation of HUWE1, and further provide a potential strategy for cancer therapy by targeting HUWE1 and the CUL4B E3 ligase complex.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
6.
PAPER CURRENT
Characterization of two 2-isopropylmalate synthase homologs from Thermus thermophilus HB27 (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Ayako Yoshida, Saori Kosono, Makoto Nishiyama 2-Isopropylmalate synthase (IPMS) catalyzes the first step of leucine biosynthesis and is regulated via feedback inhibition by leucine. The thermophilic bacterium, Thermus thermophilus HB27, has two IPMS homologous genes: TTC0847 and TTC0849 , both of which are in the branched-chain amino acid biosynthetic gene cluster. Since enzymes involved in the leucine biosynthetic pathway are evolutionarily related to those in isoleucine biosynthesis, TTC0847 and TTC0849 are expected to function as IPMS or citramalate synthase, which is the first enzyme in the isoleucine biosynthetic pathway from pyruvate. We characterized these proteins in vitro and in vivo , and revealed that TTC0849 plays a key role in the biosynthesis of leucine and isoleucine, whereas TTC0847 is only involved in that of isoleucine.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
7.
PAPER CURRENT
A new strategy to identify hepatitis B virus entry inhibitors by AlphaScreen technology targeting the envelope-receptor interaction (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Wakana Saso, Senko Tsukuda, Hirofumi Ohashi, Kento Fukano, Ryo Morishita, Satoko Matsunaga, Mio Ohki, Akihide Ryo, Sam-Yong Park, Ryosuke Suzuki, Hideki Aizaki, Masamichi Muramatsu, Camille Sureau, Takaji Wakita, Tetsuro Matano, Koichi Watashi Current anti-hepatitis B virus (HBV) agents have limited effect in curing HBV infection, and thus novel anti-HBV agents with different modes of action are in demand. In this study, we applied AlphaScreen assay to high-throughput screening of small molecules inhibiting the interaction between HBV large surface antigen (LHBs) and the HBV entry receptor, sodium taurocholate cotransporting polypeptide (NTCP). From the chemical screening, we identified that rapamycin, an immunosuppressant, strongly inhibited the LHBs-NTCP interaction. Rapamycin inhibited hepatocyte infection with HBV without significant cytotoxicity. This activity was due to impaired attachment of the LHBs preS1 domain to cell surface. Pretreatment of target cells with rapamycin remarkably reduced their susceptibility to preS1 attachment, while rapamycin pretreatment to preS1 did not affect its attachment activity, suggesting that rapamycin targets the host side. In support of this, a surface plasmon resonance analysis showed a direct interaction of rapamycin with NTCP. Consistently, rapamycin also prevented hepatitis D virus infection, whose entry into cells is also mediated by NTCP. We also identified two rapamycin derivatives, everolimus and temsirolimus, which possessed higher anti-HBV potencies than rapamycin. Thus, this is the first report for application of AlphaScreen technology that monitors a viral envelope-receptor interaction to identify viral entry inhibitors.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
8.
PAPER CURRENT
miR-411 suppresses acute spinal cord injury via downregulation of Fas ligand in rats (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2 Author(s): Zong-ming Gong, Zhen-yu Tang, Xiao-liang Sun Objective To explore the role of miR-411/FasL in acute spinal cord injury (ASCI). Methods The ASCI rat model was established, and expression of miR-411 and Fas ligand (FasL) was examined. Basso, Beattie and Bresnahan (BBB) score was used to evaluate the rats' neurological function. PC12 oxygen-glucose deprivation (OGD) model was also established. Gene manipulation (including miR-411 mimic or inhibitor) was used to modulate gene expression. Luciferase reporter assay was conducted to confirm the targeting relationship between miR-411 and FasL. Flow cytometry was applied in the measurement of PC12 cell apoptosis. Finally, the miR-411 mimic was injected into the vertebral canal of ASCI rats to determine the effects of miR-411 in vivo . Results Compared with sham group, the expression of miR-411 and FasL was significantly decreased and increased in ASCI group, respectively ( P  < 0.05). Similarly, the expression of miR-411 and FasL was significantly lower and higher in OGD group than that in control group, respectively ( P  < 0.05). miR-411 directly controlled the FasL expression. miR-411 mimic can dramatically reduce the increased percentage of apoptosis cells caused by OGD when comparing to mimic control, which was greatly reversed by the overexpression of FasL ( P  < 0.05). Further, the BBB score was significantly elevated in the miR-411 mimic group when comparing to mimic control group, with decreased FasL expression ( P  < 0.05). Conclusion miR-411 mimic suppressed PC12 cell apoptosis via FasL, and relieved ASCI in rats.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
9.
PAPER CURRENT
Publication Date: 2018-05-20
Description: Publication date: 22 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 2
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
10.
PAPER CURRENT
Reduced RAR-β gene expression in Benzo(a)Pyrene induced lung cancer mice is upregulated by DOTAP lipo-ATRA treatment (2018)
Elsevier
Publication Date: 2018-05-20
Description: Publication date: 20 August 2018 Source: Gene, Volume 668 Author(s): S. Viswanathan, V.M. Berlin Grace Molecular targeted therapy for specific genes is an emerging research. Retinoic Acid Receptor (RAR-β) is a key tumor suppressor which is found to be lost drastically during much cancer progression. We hence, analyzed the expression level of RAR-β gene during B(a)P induced lung cancer development in mice and studied the lung cancer targeted action of All Trans Retinoic Acid (ATRA) in DOTAP liposomal formulation. The effect of its treatment on lung cancer was determined by histopathological analysis. RAR-β gene expression was assessed by RT-PCR and qPCR. A distinct band for RAR-β gene (density - 0.5123 for lung and 0.5160 for liver) was observed in normal mice, whereas no visible band was observed in cancer induced group, indicating loss of RAR-β gene expression. Both ATRA and lipo-ATRA treated groups showed detectable RAR-β expression with relatively lesser density than the normal group. The expression was more intense in lipo-ATRA treatment (density-0.2973) compared with free ATRA treatment (density-0.1549) in lung tissues. The qPCR results also have highlighted a highly significant ( p  ≤ 0.01) variation RQ values between lipo-ATRA group (15.46 ± 1.54) and free ATRA group (7.58 ± 1.30) in lung tissue sample on 30th day. The mean RQ value for normal lung on 30th day was 20.86 ± 2.58 against the cancer control. The 120th day mice also showed the similar RAR-β expression pattern with further declined expression levels as there was no treatment given after 30 days. Interestingly, the lipo-ATRA treatment could show a highly significant ( p  ≤ 0.001) expression (12.00 ± 2.31) when compared with free ATRA treatment (3.31 ± 0.58) which implies that the lipo-ATRA formulation could result in sustained delivery of ATRA in target site. Histopathology of lung and liver on 120th day also revealed an effective therapeutic indication in lipo-ATRA treatment compared to free ATRA treatment due to lipo-ATRA's stealth property and it efficiently inhibited the metastasis to liver. These results revealed that the lipo-ATRA treatment has efficiently delivered ATRA into target site than free ATRA and in-turn it might have induced the expression of RAR-β gene or prevented loss of RAR-β gene in cancer animals.
Print ISSN: 0378-1119
Electronic ISSN: 1879-0038
Topics: Biology
Published by Elsevier