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Jianguo Chen

Publications and source records attributed to Jianguo Chen.

33 records · Page 2Linked to original sources
PubMed2004

Two variants of the human hepatocellular carcinoma-associated HCAP1 gene and their effect on the growth of the human liver cancer cell line Hep3B.

We have cloned a cDNA from chromosome band 17p13.3, designated as HCAP1 (HCC-associated protein 1, originally named HC56). Database searches revealed that HCAP1 shares most of its open reading frame with GEMIN4. Single nucleotide polymorphism (SNP) screening revealed a high incidence of SNP in the coding region of HCAP1 (12 SNP sites). A collection of 140 controls and 22 cases from the Qidong area was genotyped at 6 SNP sites. The 22 cases exhibited higher frequencies of minor alleles than did the controls, and 2 sites revealed significant differences between the controls and the cases. We constructed 2 haplotypes, HCAP1-N (with common alleles at 5 SNP sites) and HCAP1-M (with minor alleles at 5 SNP sites), in a mammalian expression system. Both haplotypes resulted in a remarkable reduction in colony formation and suppression of cell growth after being transfected into the human hepatocellular carcinoma (HCC) cell line. The inhibitory effect of HCAP1-N was stronger than that of HCAP1-M. Different haplotypes also resulted in different gene expression profiles in the Hep3B cell line according to an examination of 588 genes on an Atlas membrane. The expression induced by HCAP1-M caused an up-regulation of genes involved in cellular proliferation and a down-regulation of genes involved in cellular apoptosis and DNA repair. These results, in addition to the statistical data, are biological evidence that the HCAP1-M variant of HCAP1 has a reduced inhibitory effect on hepatocarcinoma cell growth and an impaired DNA repair system. This suggests that HCAP1-M may be related to cancer susceptibility.

Alleles↗
PubMed2004

The beta1 subunit enhances oxidative regulation of large-conductance calcium-activated K+ channels.

Oxidative stress may alter the functions of many proteins including the Slo1 large conductance calcium-activated potassium channel (BKCa). Previous results demonstrated that in the virtual absence of Ca2+, the oxidant chloramine-T (Ch-T), without the involvement of cysteine oxidation, increases the open probability and slows the deactivation of BKCa channels formed by human Slo1 (hSlo1) alpha subunits alone. Because native BKCa channel complexes may include the auxiliary subunit beta1, we investigated whether beta1 influences the oxidative regulation of hSlo1. Oxidation by Ch-T with beta1 present shifted the half-activation voltage much further in the hyperpolarizing direction (-75 mV) as compared with that with alpha alone (-30 mV). This shift was eliminated in the presence of high [Ca2+]i, but the increase in open probability in the virtual absence of Ca2+ remained significant at physiologically relevant voltages. Furthermore, the slowing of channel deactivation after oxidation was even more dramatic in the presence of beta1. Oxidation of cysteine and methionine residues within beta1 was not involved in these potentiated effects because expression of mutant beta1 subunits lacking cysteine or methionine residues produced results similar to those with wild-type beta1. Unlike the results with alpha alone, oxidation by Ch-T caused a significant acceleration of channel activation only when beta1 was present. The beta1 M177 mutation disrupted normal channel activation and prevented the Ch-T-induced acceleration of activation. Overall, the functional effects of oxidation of the hSlo1 pore-forming alpha subunit are greatly amplified by the presence of beta1, which leads to the additional increase in channel open probability and the slowing of deactivation. Furthermore, M177 within beta1 is a critical structural determinant of channel activation and oxidative sensitivity. Together, the oxidized BKCa channel complex with beta1 has a considerable chance of being open within the physiological voltage range even at low [Ca2+]i.

Cell Line↗
PubMed2003

Biosynthesis, purification, and substrate specificity of severe acute respiratory syndrome coronavirus 3C-like proteinase.

The 3C-like proteinase of severe acute respiratory syndrome (SARS) coronavirus has been proposed to be a key target for structural-based drug design against SARS. In order to understand the active form and the substrate specificity of the enzyme, we have cloned, expressed, and purified SARS 3C-like proteinase. Analytic gel filtration shows a mixture of monomer and dimer at a protein concentration of 4 mg/ml and mostly monomer at 0.2 mg/ml, which correspond to the concentration used in the enzyme assays. The linear decrease of the enzymatic-specific activity with the decrease of enzyme concentration revealed that only the dimeric form is active and the dimeric interface could be targeted for structural-based drug design against SARS 3C-like proteinase. By using a high pressure liquid chromatography assay, SARS 3C-like proteinase was shown to cut the 11 peptides covering all of the 11 cleavage sites on the viral polyprotein with different efficiency. The two peptides corresponding to the two self-cleavage sites are the two with highest cleavage efficiency, whereas peptides with non-canonical residues at P2 or P1' positions react slower. The P2 position of the substrates seems to favor large hydrophobic residues. Secondary structure studies for the peptide substrates revealed that substrates with more beta-sheetlike structure tend to react fast. This study provides a basic understanding of the enzyme catalysis and a full substrate specificity spectrum for SARS 3C-like proteinase, which are helpful for structural-based inhibitor design against SARS and other coronavirus.

Catalysis↗
PubMed2003

RNA-dependent RNA polymerase gene sequence from foot-and-mouth disease virus in Hong Kong.

A foot-and-mouth disease virus (FMDV, HKN/2002) was isolated in Hong Kong in 2002. The nucleotide sequence of the 3D(pol) gene encoding the viral RNA-dependent RNA polymerase was determined and compared with that of the same gene from other FMDVs. The 3D(pol) gene was 1410 nucleotides in length encoding a protein of 470 amino acid residues. Sequence comparisons indicated that HKN/2002 belonged to serotype O. An evolutionary tree based on the 3D(pol) sequences of 20 FMDV isolates revealed that the nucleotide sequence of the HKN/2002 3D(pol) gene was most similar to those of isolates found in Taiwan in 1997, suggesting that they share a common ancestor. The amino acid sequence of the HKN/2002 3D(pol) gene was determined and aligned with those of representative isolates from seven other Picornaviridae genera. Eight highly conserved regions were detected, indicating a conserved functional relevance for these motifs. Alignment of 20 FMDV 3D(pol) amino acid sequences revealed a hypermutation region near the N-terminus that may help the virus evade host immune systems.

Amino Acid Motifs↗
PubMed2003

Serotype and VP1 gene sequence of a foot-and-mouth disease virus from Hong Kong (2002).

The nucleotide sequence of the VP1 coding region of foot-and-mouth disease virus (FMDV) strain HKN/2002, isolated from a disease outbreak occurring in Hong Kong in February 2002, was determined and compared with the sequences of other FMDVs. The VP1 coding region was 639 nucleotides in length and encoded a protein of 213 amino acid residues. Comparison of the VP1 nucleotide sequence with those of other isolates indicated that HKN/2002 belonged to serotype O. A VP1-based sequence similarity tree of several South-east Asian FMDV-O isolates showed that HKN/2002 was most closely related to FMDV isolates found in Hong Kong from 1991 to 1999 and Taiwan in 1997. Comparison of the amino acid sequence of the major immunogenic region of HKN/2002 with that of the serotype O vaccine strain, O1/Manisa/Turkey/69, reveals significant similarity, indicating that current serotype O vaccines may offer some degree of protection against HKN/2002.

Amino Acid Sequence↗
PubMed2003

The minimum LOH region defined on chromosome 17p13.3 in human hepatocellular carcinoma with gene content analysis.

Hepatocellular carcinoma (HCC) is one of the most common human cancers in Asia. Previous studies have shown that in addition to aberrations of the p53 gene on chromosome 17p13.1, other gene(s) on chromosome 17p13.3 may also play a role in HCC. To detect the status of loss of heterozygosity (LOH) in HCC and to determine the minimum region of LOH on 17p13.3, we analyzed 22 paired HCC and non-cancerous liver samples with 14 polymorphic markers plus TP53 (p53 gene) as a comparison. The data revealed a high level of LOH (>68%) in a minimum region between D17S1866 and D17S1574, spanning over a 1.5 Mb region. Genomic library screening using markers in the region has resulted in the isolation of a cluster of BAC/PAC clones. We created a physical map in this region. Using large-scale genome sequencing, gene annotation, cDNA screening, and exon trapping, we identified 17 known genes and 13 novel genes in the minimum region. The function of these genes was analyzed and the possibility of several putative tumor suppressor genes was discussed.

Base Sequence↗
PubMed2002

Methylation profiling of twenty promoter-CpG islands of genes which may contribute to hepatocellular carcinogenesis.

BACKGROUND: Hepatocellular carcinoma (HCC) presents one of the major health threats in China today. A better understanding of the molecular genetics underlying malignant transformation of hepatocytes is critical to success in the battle against this disease. The methylation state of C5 of the cytosine in the CpG di-nucleotide that is enriched within or near the promoter region of over 50 % of the polymerase II genes has a drastic effect on transcription of these genes. Changes in the methylation profile of the promoters represent an alternative to genetic lesions as causative factors for the tumor-specific aberrant expression of the genes. METHODS: We have used the methylation specific PCR method in conjunction with DNA sequencing to assess the methylation state of the promoter CpG islands of twenty genes. Aberrant expression of these genes have been attributed to the abnormal methylation profile of the corresponding promoter CpG islands in human tumors. RESULTS: While the following sixteen genes remained the unmethylated in all tumor and normal tissues: CDH1, APAF1, hMLH1, BRCA1, hTERC, VHL, RARbeta, TIMP3, DAPK1, SURVIVIN, p14ARF, RB1, p15INK4b, APC, RASSF1c and PTEN, varying degrees of tumor specific hypermethylation were associated with the p16INK4a, RASSF1a, CASP8 and CDH13 genes. For instance, the p16INK4a was highly methylated in HCC (17/29, 58.6%) and less significantly methylated in non-cancerous tissue (4/29. 13.79%). The RASSF1a was fully methylated in all tumor tissues (29/29, 100%), and less frequently methylated in corresponding non-cancerous tissue (24/29, 82.75%). CONCLUSIONS: Furthermore, co-existence of methylated with unmethylated DNA in some cases suggested that both genetic and epigenetic (CpG methylation) mechanisms may act in concert to inactivate the p16INK4a and RASSF1a in HCC. Finally, we found a significant association of cirrhosis with hypermethylation of the p16INK4a and hypomethylation of the CDH13 genes. For the first time, the survey was carried out on such an extent that it would not only provide new insights into the molecular mechanisms underscoring the aberrant expression of the genes in this study in HCC, but also offer essential information required for a good methylation-based diagnosis of HCC.

Adult↗
PubMed2002

Deletion of brain dystroglycan recapitulates aspects of congenital muscular dystrophy.

Fukuyama congenital muscular dystrophy (FCMD), muscle-eye-brain disease (MEB), and Walker-Warburg syndrome are congenital muscular dystrophies (CMDs) with associated developmental brain defects. Mutations reported in genes of FCMD and MEB patients suggest that the genes may be involved in protein glycosylation. Dystroglycan is a highly glycosylated component of the muscle dystrophin-glycoprotein complex that is also expressed in brain, where its function is unknown. Here we show that brain-selective deletion of dystroglycan in mice is sufficient to cause CMD-like brain malformations, including disarray of cerebral cortical layering, fusion of cerebral hemispheres and cerebellar folia, and aberrant migration of granule cells. Dystroglycan-null brain loses its high-affinity binding to the extracellular matrix protein laminin, and shows discontinuities in the pial surface basal lamina (glia limitans) that probably underlie the neuronal migration errors. Furthermore, mutant mice have severely blunted hippocampal long-term potentiation with electrophysiologic characterization indicating that dystroglycan might have a postsynaptic role in learning and memory. Our data strongly support the hypothesis that defects in dystroglycan are central to the pathogenesis of structural and functional brain abnormalities seen in CMD.

Animals↗
PubMed2002

The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory.

Many central neurons possess large acid-activated currents, yet their molecular identity is unknown. We found that eliminating the acid sensing ion channel (ASIC) abolished H(+)-gated currents in hippocampal neurons. Neuronal H(+)-gated currents and transient acidification are proposed to play a role in synaptic transmission. Investigating this possibility, we found ASIC in hippocampus, in synaptosomes, and in dendrites localized at synapses. Moreover, loss of ASIC impaired hippocampal long-term potentiation. ASIC null mice had reduced excitatory postsynaptic potentials and NMDA receptor activation during high-frequency stimulation. Consistent with these findings, null mice displayed defective spatial learning and eyeblink conditioning. These results identify ASIC as a key component of acid-activated currents and implicate these currents in processes underlying synaptic plasticity, learning, and memory.

Acid Sensing Ion Channels↗
PubMed2002

Nitric oxide augments voltage-gated P/Q-type Ca(2+) channels constituting a putative positive feedback loop.

P/Q-type Ca(2+) channels, which are postulated to play major roles in synaptic transmission, are regulated in a variety of ways. Ca(2+) currents through P/Q-type Ca(2+) channels (Ca(v)2.1/beta(1a)/alpha(2)delta) heterologously expressed in mammalian cells were recorded using the whole-cell patch clamp method. The oxidant H(2)O(2) increased the current amplitude and the effect was reversed by the reducing agent dithiothreitol (DTT). The stimulatory effect of H(2)O(2) on the Ca(2+) current was mimicked by the NO donors, SNAP, and diethylamine NONOate, and reversed by the reducing agent DTT. The presence of a soluble guanylate cyclase inhibitor did not abolish the ability of SNAP to increase the Ca(2+) current. Adenovirus-mediated overexpression of nitric oxide synthase in combination with application of the Ca(2+) ionophore A23187 also increased the Ca(2+) current amplitude and the effect was again reversed by DTT. The NOS inhibitor L-NAME abolished the stimulatory effect of A23187, and A23187 did not change the Ca(2+) currents in the cells treated with control adenovirus particles. The time course of the decline of the Ca(2+) current, but not of the Ba(2+) current, in response to repeated depolarization was markedly slowed by adenovirus-mediated overexpression of nitric oxide synthase. The results demonstrate that nitric oxide enhances the channel activity by promoting oxidation and suggest that Ca(2+), nitric oxide synthase, and nitric oxide could constitute a positive feedback loop for regulation of voltage-gated P/Q-type Ca(2+) channels.

Adenoviridae↗
PubMed2002

Association of human cholesteryl ester transfer protein-TaqI polymorphisms with serum HDL cholesterol levels in a normolipemic Japanese rural population.

We examined allele frequencies for the common cholesteryl ester transfer protein (CETP) TaqI polymorphisms and the associations of CETP-TaqI polymorphisms with serum lipid and lipoprotein levels taking into account for selected lifestyle factors in a well-characterized random sample of 527 healthy subjects living a rural community in Japan (256 men and 271 women aged 40-69 years). B2 allele frequency was 0.39 in men and 0.41 in women, and its presence was significantly associated with increased levels of HDL cholesterol (HDL-C) in men (P=0.003 for linear trend). A similar tendency in women was observed, although P value for trend did not reach 0.05. There were not significant interactions between TaqIB genotype and smoking and alcohol drinking or daily physical activity in HDL-C. There were no statistically significant differences among TaqIA genotype in lipid and lipoprotein levels. Multiple linear regression analysis showed that B1B2 and B2B2 explained 1.7% and 2.2%, and 0.6% and 1.0% of variation in men and in women in HDL-C, respectively. We conclude that the CETP-TaqIB polymorphism has a quantitative influence, but appears to be stronger one in men, on HDL-C levels even after adjustment for important lifestyle factors (smoking, alcohol drinking, and daily physical activity).

Adult↗
PubMed2001

Intracrine hepatopoietin potentiates AP-1 activity through JAB1 independent of MAPK pathway.

Many growth factors and cytokines are involved in liver regeneration. Of them, only hepatopoietin (HPO)/ALR (augmenter of liver regeneration) is a specifically hepatotrophic factor originally identified from the cytosol of regenerating or hyperplastic hepatic cells. Previous reports indicate that extracellular HPO triggers the MAPK pathway by binding its specific receptor on the cell surface. However, its function in the cytosol of hepatocytes is unclear. Here we identified that JAB1 (Jun activation domain-binding protein 1), a co-activator of AP-1, which is essential for liver regeneration, specifically interacts with intracellular HPO. JAB1 colocalizes with HPO in nuclei of hepatic cells or COS-7 cells. As an intracrine factor, the intracellular function of HPO is to increase c-Jun phosphorylation independent of c-Jun amino-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) -1 and -2, and leads to potentiation of JAB1-mediated AP-1 activation. Amino acids 1-63 of HPO molecule are sufficient to bind to JAB1, but the full-length HPO is necessary for its intracellular signaling. Taken together, these results elucidate a novel mechanism of intracrine cytokine signaling by specifically modulating the AP-1 pathway through JAB1, in a MAPK-independent fashion.

Animals↗
PubMed1996

Insertion of Fluoroalkenes into Activated C-H Bonds for the Preparation of Polyfluorinated Sulfanes, Alcohols, and Acyclic and Cyclic Ethers.

Free radical addition reactions of tetrahydrothiophene, pentamethylene sulfide, and 1,4-thioxane with various cyclic and acyclic per- and polyfluorinated olefins are readily initiated by di-tert-butyl peroxide, providing a convenient route for synthesizing cyclic sulfanes with fluorinated side groups. Tetrahydrothiophene reacts with hexafluoropropene, perfluoroallylbenzene, perfluorocyclobutene, and 1,2-dichlorotetrafluorocyclobutene in the presence of catalytic amounts of the peroxide to give the corresponding addition products CH(2)CH(2)CH(2)SCHCF(2)CHFCF(3) (1), CH(2)CH(2)CH(2)SCHCF(2)CHFCF(2)C(6)F(5) (2), CH(2)CH(2)CH(2)SCHCFCHFCF(2)CF(2) (3), and CH(2)CH(2)CH(2)SCHCClCHClCF(2)CF(2) (4), respectively. Pentamethylene sulfide reacts analogously with hexafluoropropene to give CH(2)CH(2)CH(2)CH(2)SCHCF(2)CHFCF(3) (8). Reaction of 1,4-thioxane with hexafluoropropene or perfluoroallylbenzene gives a mixture of two products, OCH(2)CH(2)SCH(2)CHCF(2)CHFCF(3) (9) and SCH(2)CH(2)OCH(2)CHCF(2)CHFCF(3) (10) or OCH(2)CH(2)SCH(2)CHCF(2)CHFCF(2)C(6)F(5) (11) and SCH(2)CH(2)OCH(2)CHCF(2)CHFCF(2)C(6)F(5) (12), respectively. Fluorinated alcohols C(6)F(5)CF(2)CHFCF(2)C(CH(3))(2)OH (15), C(6)F(5)CF(2)CHFCF(2)CH(CH(3))OH (16), and C(6)F(5)CF(2)CHFCF(2)CH(2)OH (17) are prepared by reacting perfluoroallylbenzene with the corresponding alcohols. When 15 is reacted with pentafluorobenzonitrile in the presence of potassium carbonate, an unexpected cyclic ether 19 is obtained as the major product in addition to C(6)F(5)CF(2)CHFCF(2)C(CH(3))(2)OC(6)F(5)CN (18). Alcohols 15-17 can be cyclized by heating with potassium carbonate to give fluorinated cyclic ethers 19-21. The X-ray crystal structures of acyclic ether 18 and cyclic ether 19 are given. Compound 18 crystallizes in the tetragonal system, space group P4(2)/n, with a = 18.471(0) Å, b = 18.471(0) Å, c = 11.702(0) Å, V = 3992.5(9) Å(3), D(calc) = 1.768 mg/m(3), Z = 8, and R = 0.0617. Compound 19 crystallizes in the triclinic system, space group P&onemacr;, with a = 8.103(3) Å, b = 8.790(3) Å, c = 9.832(3) Å, alpha = 66.25(4) degrees, beta = 72.01(3) degrees, gamma = 80.19(4) degrees, V = 608.7(4) Å(3), D(calc) = 1.845 mg/m(3), Z = 2, and R = 0.0346.

Journal Article↗
PubMed1996

Synthesis of Cyclic Ethers with Fluorinated Side Chains.

Di-tert-butyl peroxide initiated free radical addition of THF to various fluorinated alkenes (CF(2)=CH(2), CF(2)=CFH, CH(2)=CHCF(3), CF(2)=CFCF(3), CF(2)=CFC(5)F(11), CF(2)=CFOCF(2)CF(CF(3))OCF(2)CF(2)SO(2)F) gives either bidirectional addition products [CH(2)CH(2)CH(2)OCH(CF(2)CH(3)) (1), CH(2)CH(2)CH(2)OCH(CH(2)CHF(2)) (2), CH(2)CH(2)CH(2)OCH(CF(2)CH(2)F) (3), and CH(2)CH(2)CH(2)OCH(CFHCHF(2)) (4)] or unidirectional products [CH(2)CH(2)CH(2)OCH(CH(2)CH(2)CF(3)) (5), CH(2)CH(2)CH(2)OCH(CF(2)CHFCF(3)) (6), CH(2)CH(2)CH(2)OCH(CF(2)CHFC(5)F(11)) (7), and CH(2)CH(2)CH(2)OCH(CF(2)CHFOCF(2)CF(CF(3))OCF(2)CF(2)SO(2)F) (8)] depending on the structure of the alkene. Reaction of dioxane with CF(2)=CFOCF(2)CF(CF(3))OCF(2)CF(2)SO(2)F gives a single product, CH(2)OCH(2)CH(2)OCH(CF(2)CHFOCF(2)CF(CF(3))OCF(2)CF(2)SO(2)F) (9). In the case of hexafluoropropene or perfluoroallylbenzene, reaction with an excess of tetrahydrofuran gives only the monosubstituted products CH(2)CH(2)CH(2)OCH(CF(2)CHFCF(3)) (6) and CH(2)CH(2)CH(2)OCH(CF(2)CFHCF(2)C(6)F(5)) (11) respectively. When tetrahydrofuran is reacted with a 3:1 molar excess of the same two perfluoroalkenes, the disubstituted products CH(2)CH(2)CH(CF(2)CHFCF(3))OCH(CF(2)CHFCF(3)) (10) and CH(2)CH(2)CH(CF(2)CFHCF(2)C(6)F(5))OCH(CF(2)CFHCF(2)C(6)F(5)) (12) are formed respectively. When 18-crown-6 is reacted in the same way with fluoroalkenes in a 1:1 molar ratio, the monosubstituted products 18-crown-6-CH(2)CH(2)CF(3) (13), 18-crown-6-CF(2)CHFCF(3) (14), 18-crown-6-CF(2)CFHCF(2)C(6)F(5) (15), and 18-crown-6-CF(2)CHFOCF(2)CF(CF(3))OCF(2)CF(2)SO(2)F (16) are obtained. Polyfluorinated 18-crown-6 products containing three and two polyfluroalkyl/aryl groups are prepared when 18-crown-6 is reacted with a 3:1 molar excess of perfluoropropene and perfluoroallylbenzene to give 18-crown-6-(CF(2)CHFCF(3))(3) (17) and 18-crown-6-(CF(2)CFHCF(2)C(6)F(5))(2) (18), respectively. (Pentafluorophenoxy)trimethylsilane reacts with 11 in the presence of a catalytic amount of cesium fluoride to give compound 19, CH(2)CH(2)CH(2)OCH(CF(2)CFHCF(2)C(6)F(4)OC(6)F(5)). Two molecules of 11 are bridged by reaction with Me(3)SiOCH(2)CF(2)CF(2)CF(2)CH(2)OSiMe(3) to give CH(2)CH(2)CH(2)OCHCF(2)CFHCF(2)C(6)F(4)OCH(2)CF(2)CF(2)CF(2)CH(2)OC(6)F(4)CF(2)CHFCF(2)CHOCH(2)CH(2)CH(2) (20), while 12 forms the macroheterocycle OCHCH(2)CH(2)CHCF(2)CFHCF(2)C(6)F(4)OCH(2)CF(2)CF(2)CF(2)CH(2)OC(6)F(4)CF(2)CFHCF(2) (21) under similar reaction conditions. The lanthanum triflate complexes of 18-crown-6 (22) and 18-crown-6(CF(2)CFHCF(3)) (23) were prepared and the structures were obtained via single-crystal X-ray analysis. Although crystals suitable for single-crystal X-ray analysis could not be formed, lanthanum triflate complexes were formed with polyfluorinated ethers 15 and 16 to give the fluorinated complexes La(OSO(2)CF(3))(3)(18-crown-6-CF(2)CFHCF(2)C(6)F(5))(H(2)O) (24) and [La(OCH(2)CH(2))(5)OCH(2)CHCF(2)CFHOCF(2)C(CF(3))FOCF(2)CF(2)SO(2)F](3+)[CF(3)SO(3)(-)](3) (25) respectively. The acid salt La[N(SO(2)CF(3))(2)](3) (26) was also prepared and characterized, and reacted with dibenzo-18-crown-6 to give the complex dibenzo-18-crown-6-La[N(SO(2)CF(3))(2)](3) (27).

Journal Article↗