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1.
G. Mattson E. Conklin S. Desai G. Nielander M. D. Savage S. Morgensen 《Molecular biology reports》1993,17(3):167-183
The various aspects of chemical crosslinking are addressed. Crosslinker reactivity, specificity, spacer arm length and solubility characteristics are detailed. Considerations for choosing one of these crosslinkers for a particular application are given as well as reaction conditions and practical tips for use of each category of crosslinkers.Abbreviations ABH
azidobenzoyl hydrazide
- ANB- NOS
N-5-azido-2-nitrobenzoyloxysuccinimide
- ASIB
1-(p-azidosalicylamido)-4-(iodoacetamido)butane
- ASBA
4-(p-azidosalicylamido)butylamine
- APDP
N-[4-(p-azidosalicylamido) butyl]-3(2-pyridyldithio)propionamide
- APG
p-azidophenyl glyoxal monohydrate
- BASED
bis-[-(4-azidosalicylamido)ethyl] disulfide
- BMH
bismaleimidohexane
- BS3
bis(sulfosuccinimidyl) suberate
- BSOCOES
bis[2-(succinimidooxycarbonyloxy)ethyl]sulfone
- DCC
N,N-dicyclohexylcarbodiimide
- DFDNB
1,5-difluoro-2,4-dinitrobenzene
- DMA
dimethyl adipimidate·2HCl
- DMP
dimethyl pimelimidate·2HCl
- DMS
dimethyl suberimidate·2HCl
- DPDPB
1,4-di-(3,2-pyridyldithio)propionamido butane
- DMF
dimethylformamide
- DMSO
dimethylsulfoxide
- DSG
disuccinimidyl glutarate
- DSP
dithiobis(succinimidylpropionate)
- DSS
disuccinimidyl suberate
- DST
disuccinimidyl tartarate
- DTSSP
3,3-dithiobis (sulfosuccinimidylpropionate)
- DTBP
dimethyl 3,3-dithiobispropionimidate·2HCl
- EDC or EDAC
1-ethyl-3-(3-dimethylaminopropyl)carbodimide hydrochloride
- EDTA
ethylenediaminetetraacetic acid disodium salt, dihydrate
- EGS
ethylene glycolbis(succinimidylsuccinate)
- GMBS
N--maleimidobutyryloxysuccinimide ester
- HSAB
N-hydroxysuccinimidyl-4-azidobenzoate
- HEPES
4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid
- MBS
m-maleimidobenzoyl-N-hydroxysuccinimide ester
- MES
4-morpholineethanesulfonic acid
- NHS
N-hydroxysuccinimide
- NHS-ASA
N-hydroxysuccinimidyl-4-azidosalicylic acid
- PMFS
phenylmethylsulfonyl fluoride
- PNP-DTP
p-nitrophenyl-2-diazo-3,3,3-trifluoropropionate
- SAED
sulfosuccinimidyl 2-(7-azido-4-methylcoumarin-3-acetamide) ethyl-1,3-dithiopropionate
- SADP
N-succinimdyl (4-azidophenyl)1,3-dithiopropionate
- SAND
sulfosuccinimidyl 2-(m-azido-o-nitrobenzamido)-ethyl-1,3-dithiopropionate
- SANPAH
N-succinimidyl-6(4-azido-2-nitrophenyl-amino)hexanoate
- SASD
sulfosuccinimidyl 2-(p-azidosalicylamido)ethyl-1,3-dithiopropionate
- SATA
N-succinimidyl-S-acetylthioacetate
- SDBP
N-hydroxysuccinimidyl-2,3-dibromopropionate
- SIAB
N-succinimidyl(4-iodoacetyl)aminobenzoate
- SMCC
succinimidyl 4-(N-maleimidomethyl)cyclohexane-1-carboxylate
- SMPB
succinimidyl 4-(p-maleimidophenyl) butyrate
- SMPT
4-succinimidyloxycarbonyl--methyl--(2-pyridyldithio)-toluene
- sulfo-BSOCOES
bis[2-sulfosuccinimidooxycarbonyloxy) ethyl]sulfone
- sulfo-DST
disulfosuccinimidyl tartarate
- sulfo-EGS
ethylene glycolbis(sulfosuccinimidylsuccinate)
- sulfo-GMBS
N--maleimidobutyryloxysulfosuccinimide ester
- sulfo-MBS
m-maleimidobenzoyl-N-hydroxysulfosuccinimide ester
- sulfo-SADP
sulfosuccinimidyl(4-azidophenyldithio)propionate
- sulfo-SAMCA
sulfosuccinimidyl 7-azido-4-methylcoumarin-3-acetate
- sulfo-SANPAH
sulfosuccinimidyl 6-(4-azido-2-nitrophenylamino)hexanoate
- sulfo-SIAB
sulfosuccinimidyl(4-iodoacetyl)aminobenzoate
- sulfo-SMPB
sulfo-succinimidyl 4-(p-maleimidophenyl)butyrate
- sulfo-SMCC
sulfosuccinimidyl 4-(N-maleimidomethyl)cyclohexane-1-carboxylate
- SPDP
N-succinimidyl 3-(2-pyridyldithio)propionate 相似文献
2.
3.
4.
Sperm whale apomyoglobin was reconstituted with selectively deuterated D6-2,4-diacetyldeuterohemin in which the 2H label was confined to the methyl groups of the acetyl moieties. A single resonance was observed in 2H NMR of the cyanoferrimyoglobin derivative, with a chemical shift 0.80 ppm downfield of external D12-TMS at pH 6.7. The corresponding chemical shift of D6-2,4-diacetyldeuterohemin-OMe as the cyanide complex in pyridine-water was 0.96 ppm downfield of external D12-TMS. The prominent HOD peak was well separated at 4.4 ppm downfield. The line width of the porphyrin 2H resonances in both the protein and free solvent environments yields evidence of considerable rotational freedom of the -CD3 groups about their axes. 相似文献
5.
6.
Raveendra Melavanki Kalpana Sharma Basappa Chanabasapa Yallur Raviraj Kusanur Kishor Kumar Sadasivuni Diksha Singh Smita Mane Kariyappa Katagi Shridhar V. Pattar 《Luminescence》2021,36(1):163-168
Continuous monitoring of glucose and sugar sensing plays a vital role in diabetes control. The drawbacks of the present enzyme‐based sugar sensors have encouraged the investigation into alternate approaches to design new sensors. The popularity of fluorescence sensors is due to their ability to bind reversibly to compounds containing diol. In this study we investigated the binding ability of phenyl boronic acid P1 for monosaccharides and disaccharides (sugars) in aqueous medium at physiological pH 7.4 using steady‐state fluorescence and absorbance. P1 fluorescence was quenched due to formation of esters with sugars. Absorbance and fluorescence measurements led to results that indicated that the sugars studied could be ordered in terms of their affinity to P1, as stated: sucrose > lactose > galactose > xylose > ribose > arabinose. In each case, the slope of modified Stern–Volmer plots was nearly 1, indicating the presence of only a single binding site in boronic acids for sugars. Docking studies were carried out using Schrodinger Maestro v.11.2 software. The binding affinity of phenyl boronic acid P1 with periplasmic protein (PDB ID 2IPM and 2IPL) was estimated using GlideScore. 相似文献
7.
Hideaki Tagashira Chen Zhang Ying-mei Lu Hideyuki Hasegawa Hiroshi Kanai Feng Han Kohji Fukunaga 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
We previously reported that the σ1-receptor (σ1R) is down-regulated following cardiac hypertrophy and dysfunction in transverse aortic constriction (TAC) mice. Here we address how σ1R stimulation with the selective σ1R agonist SA4503 restores hypertrophy-induced cardiac dysfunction through σ1R localized in the sarcoplasmic reticulum (SR).Methods
We first confirmed anti-hypertrophic effects of SA4503 (0.1–1 μM) in cultured cardiomyocytes exposed to angiotensin II (Ang II). Then, to confirm the ameliorative effects of σ1R stimulation in vivo, we administered SA4503 (1.0 mg/kg) and the σ1R antagonist NE-100 (1.0 mg/kg) orally to TAC mice for 4 weeks (once daily).Results
σ1R stimulation with SA4503 significantly inhibited Ang II-induced cardiomyocyte hypertrophy. Ang II exposure for 72 h impaired phenylephrine (PE)-induced Ca2 + mobilization from the SR into both the cytosol and mitochondria. Treatment of cardiomyocytes with SA4503 largely restored PE-induced Ca2 + mobilization into mitochondria. Exposure of cardiomyocytes to Ang II for 72 h decreased basal ATP content and PE-induced ATP production concomitant with reduced mitochondrial size, while SA4503 treatment completely restored ATP production and mitochondrial size. Pretreatment with NE-100 or siRNA abolished these effects. Chronic SA4503 administration also significantly attenuated myocardial hypertrophy and restored ATP production in TAC mice. SA4503 administration also decreased hypertrophy-induced impairments in LV contractile function.Conclusions
σ1R stimulation with the specific agonist SA4503 ameliorates cardiac hypertrophy and dysfunction by restoring both mitochondrial Ca2 + mobilization and ATP production via σ1R stimulation.General significance
Our observations suggest that σ1R stimulation represents a new therapeutic strategy to rescue the heart from hypertrophic dysfunction. 相似文献8.
Phenyl 2‐pyridyl ketoxime induces cellular senescence‐like alterations via nitric oxide production in human diploid fibroblasts
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Kyeong Eun Yang Hyun‐Jin Jang In‐Hu Hwang Young‐Ho Chung Jong‐Soon Choi Tae‐Hoon Lee Yun‐Jo Chung Min‐Seung Lee Mi Young Lee Eui‐Ju Yeo Ik‐Soon Jang 《Aging cell》2016,15(2):245-255
Phenyl‐2‐pyridyl ketoxime (PPKO) was found to be one of the small molecules enriched in the extracellular matrix of near‐senescent human diploid fibroblasts (HDFs). Treatment of young HDFs with PPKO reduced the viability of young HDFs in a dose‐ and time‐dependent manner and resulted in senescence‐associated β‐galactosidase (SA‐β‐gal) staining and G2/M cell cycle arrest. In addition, the levels of some senescence‐associated proteins, such as phosphorylated ERK1/2, caveolin‐1, p53, p16ink4a, and p21waf1, were elevated in PPKO‐treated cells. To monitor the effect of PPKO on cell stress responses, reactive oxygen species (ROS) production was examined by flow cytometry. After PPKO treatment, ROS levels transiently increased at 30 min but then returned to baseline at 60 min. The levels of some antioxidant enzymes, such as catalase, peroxiredoxin II and glutathione peroxidase I, were transiently induced by PPKO treatment. SOD II levels increased gradually, whereas the SOD I and III levels were biphasic during the experimental periods after PPKO treatment. Cellular senescence induced by PPKO was suppressed by chemical antioxidants, such as N‐acetylcysteine, 2,2,6,6‐tetramethylpiperidinyloxy, and L‐buthionine‐(S,R)‐sulfoximine. Furthermore, PPKO increased nitric oxide (NO) production via inducible NO synthase (iNOS) in HDFs. In the presence of NOS inhibitors, such as L‐NG‐nitroarginine methyl ester and L‐NG‐monomethylarginine, PPKO‐induced transient NO production and SA‐β‐gal staining were abrogated. Taken together, these results suggest that PPKO induces cellular senescence in association with transient ROS and NO production and the subsequent induction of senescence‐associated proteins . 相似文献
9.
Robert H. White 《Chirality》1996,8(4):332-340
The configuration at the C-9 of methanopterin (MPT) has been determined by comparing the circular dichroism (CD) spectra of MPT and its hydrolytic fragment, 1-[4-[[1-(2-amino-7-methyl-4-hydroxy-6-pteridinyl)-ethyl]amino]phenyl]-1-deoxy-D -ribitol (HP-1), with the CD spectra of a series of model compounds of known stereochemistry. These compounds included (S)-6-[1-(4-carboxymethylanilino)ethyl]pterin, (S-6(1-hydroxyethyl)-7-methylpterin, (S-6-(1-hydroxyethyl)pterin, (R)-6-(1-phenoxyethyl)pterin, D (+)-neopterin, and L -biopterin. From this comparison it was concluded that MPT has the R configuration at C-9 and is thus configurationally related to D (+)-neopterin, which has the S configuration at C-1. From previous work establishing the relative stereochemistry at C-6, C-7, and C-9 of N5-N10-methenyl-5,6,7,8-tetrahydromethanopterin (N5-N10-methenyl-H4MPT) as R, S, and R, respectively, it is clear that the remaining asymmetric carbons at C-6 and C-7 of H4MPT have the S and S configuration, respectively. Comparison of these latter two positions to the equivalent carbons in 5,6,7,8-tetrahydrofolate (H4folate) show that the steps involved in the biological reduction of MPT to H4MPT occur with the same stereochemical outcome as those involved in the biological reduction of folate to H4folate. © 1996 Wiley-Liss, Inc. 相似文献
10.
Cheshev P. E. Kononov L. O. Tsvetkov Yu. E. Shashkov A. S. Nifantiev N. E. 《Russian Journal of Bioorganic Chemistry》2002,28(5):419-429
The synthesis of thioglycoside glycosyl donors with a disaccharide -D-Gal-(1 3)-D-GalNAc backbone was studied using the glycosylation of a series of suitably protected 3-monohydroxy- and 3,4-dihydroxyderivatives of phenyl 2-azido-2-deoxy-1-thio-- and 1-thio--D-galactopyranosides by galactosyl bromide, fluoride, and trichloroacetimidate. In the reaction with the monohydroxylated glycosyl acceptor, the process of intermolecular transfer of thiophenyl group from the glycosyl acceptor onto the cation formed from the molecule of glycosyl donor dominated. When glycosylating 3,4-diol under the same conditions, the product of the thiophenyl group transfer dominated or the undesired (1 4), rather than (1 3)-linked, disaccharide product formed. The aglycon transfer was excluded when 4-nitrophenylthio group was substituted for phenylthio group in the galactosyl acceptor molecule. This led to the target disaccharide, 4-nitrophenyl 2-azido-4,6-O-benzylidene-2-deoxy-3-O-(2,3,4,6-tetra-O-acetyl--D-galactopyranosyl)-1-thio--D-galactopyranoside, in 57% yield. This disaccharide product bears nonparticipating azido group in position 2 of galactosamine and can hence be used to form -glycoside bond. Azido group and the aglycon nitro group were simultaneously reduced in this product and then trichloroacetylated, which led to the -glycosyl donor, 4-trichloroacetamidophenyl 4,6-di-O-acetyl-2-deoxy-3-O-(2,3,4,6-tetra-O-acetyl--D-galactopyranosyl)-1-thio-2-trichloroacetamido--D-galactopyranoside, in 62% yield. The resulting glycosyl donor was used in the synthesis of tetrasaccharide asialo-GM1. 相似文献