Selectively recognizing extrahelical conformations of DNA trinucleotide repeats by a hydroxylated porphyrin ligand

Tetra(2,4,6 triisopropropyl phenyl)porphyrinatorhodium(II) ((TTiPP)RhII·1) is a persistent metal-centered radical with the odd electron in the rhodium(II) dz2 orbital. (TTiPP)RhII· forms 1:1 complexes with CO and CH2CH2 where the porphyrin ligand steric properties inhibit further reactions of the one-electron activated substrates. 1H NMR paramagnetic shifts at a series of temperatures are used in evaluating the thermodynamics for CO complex formation with 1 to form [(TTiPP)RhII(CO)]·2 (ΔH° = -5.5 ± 0.5 kcal mol-1; ΔS° = -9 ± 1 cal K-1 mol-1). Related 1H NMR studies show that the bonding of 1 with ethene is less favorable than CO.Key words: rhodium porphyrin, carbon monoxide, ethene, thermodynamics, complex formation, metal-centered radical.

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Metal Complexes with Tetrapyrrole Ligands, XLV. The Mercuration of Nickel(II), Palladium(II), and Platinum(II) Porphyrins

Zeitschrift für Naturforschung B ◽

10.1515/znb-1987-0813 ◽

1987 ◽

Vol 42 (8) ◽

pp. 1003-1008 ◽

Cited By ~ 9

Author(s):

Johann W. Buchler ◽

Gerhard Herget

Keyword(s):

Sodium Chloride ◽

Metal Complexes ◽

Negative Charge ◽

Mercuric Acetate ◽

Reaction Times ◽

Total Density ◽

Electrophilic Attack ◽

Aqueous Sodium ◽

Porphyrin Ligand ◽

Rapid Reaction

AbstractThe mercuration of 5,10,15,20-tetrakis(4-methylphenyl)porphyrin complexes M(TTP)** (2a-c; M = Ni, Pd, Pt) is described. Treatment of Ni(TTP) (2a) with mercuric acetate in refluxing benzene and subsequently with aqueous sodium chloride yields a mixture of species M(TTP-HgnIn) (1 < n < 3) from which the monomercurial, Ni(TTP-HgCl) (3a) is isolated in 35% yield after silica chromatography. A more rapid reaction occurs with mercuric trifluoroacetate in chlorobenzene. With this system, Pd(TTP-HgCl) (3b) and Pt(TTP-HgCl) (3c) along with their bis-, tris-, and tetrakis-mercurated analogs are obtained. The reaction times indicate that replacement of NiII by PdII and PtII progressively diminishes the rate of electrophilic attack at the porphyrin periphery, consistent with a decrease of the total density of negative charge on the porphyrin ligand in these complexes.

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Huntington's Disease: An Immune Perspective

Neurology Research International ◽

10.1155/2011/563784 ◽

2011 ◽

Vol 2011 ◽

pp. 1-7 ◽

Cited By ~ 12

Author(s):

Annapurna Nayak ◽

Rafia Ansar ◽

Sunil K. Verma ◽

Domenico Marco Bonifati ◽

Uday Kishore

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Neurodegenerative Disorder ◽

Typical Feature ◽

Trinucleotide Repeats ◽

Mutant Huntingtin Protein ◽

Unexplored Area ◽

Cag Trinucleotide Repeats ◽

The Brain ◽

Abnormal Expansion

Huntington's disease (HD) is a progressive neurodegenerative disorder that is caused by abnormal expansion of CAG trinucleotide repeats. Neuroinflammation is a typical feature of most neurodegenerative diseases that leads to an array of pathological changes within the affected areas in the brain. The neurodegeneration in HD is also caused by aberrant immune response in the presence of aggregated mutant huntingtin protein. The effects of immune activation in HD nervous system are a relatively unexplored area of research. This paper summarises immunological features associated with development and progression of HD.

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