Experimentally calibrated computational chemistry of tryptophan hydroxylase: Trans influence, hydrogen-bonding, and 18-electron rule govern O2-activation

2010 ◽  
Vol 104 (2) ◽  
pp. 136-145 ◽  
Author(s):  
Lærke T. Haahr ◽  
Kasper P. Jensen ◽  
Jane Boesen ◽  
Hans E.M. Christensen
Keyword(s):  
Hydrogen Bonding ◽  
Computational Chemistry ◽  
Tryptophan Hydroxylase ◽  
O2 Activation ◽  
Trans Influence

Charge-assisted hydrogen bonding in salts of 2-amino-1H-benzimidazole with 3-phenylpropynoic acid and oct-2-ynoic acid

2015 ◽  
Vol 71 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Charmaine Arderne ◽  
Denise K. Olivier ◽  
Derek T. Ndinteh
Keyword(s):  
Crystal Structure ◽  
Hydrogen Bonding ◽  
Computational Chemistry ◽  
Ion Pairs ◽  
Monoclinic Symmetry ◽  
Space Group ◽  
Symmetry Space ◽  
Graph Sets ◽  
Symmetry Space Group ◽  
Hydrogen Bonded

The 100 K structures of two salts, namely 2-amino-1H-benzimidazolium 3-phenylpropynoate, C7H8N3+·C9H5O2−, (I), and 2-amino-1H-benzimidazolium oct-2-ynoate, C7H8N3+·C8H11O2−, (II), both have monoclinic symmetry (space groupP21/c) and display N—H...O hydrogen bonding. Both structures show packing with corrugated sheets of hydrogen-bonded molecules lying parallel to the [001] direction. Two hydrogen-bonded ring motifs can be identified and described with graph setsR22(8) andR44(16), respectively, in both (I) and (II). Computational chemistry calculations performed on both compounds show that the hydrogen-bonded ion pairs are more energetically favourable in the crystal structure than their hydrogen–bonded neutral molecule counterparts.

Hydrogen bonding in liquid methanol at ambient conditions and at high pressure

2000 ◽  
Vol 98 (3) ◽  
pp. 125-134 ◽  
Author(s):  
T. Weitkamp, J. Neuefeind, H. E. Fisch
Keyword(s):  
High Pressure ◽  
Hydrogen Bonding ◽  
Ambient Conditions

Serotonergic Genes and Suicidality

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 54-60 ◽  
Author(s):  
Lisheng Du ◽  
Gabor Faludi ◽  
Miklos Palkovits ◽  
David Bakish ◽  
Pavel D. Hrdina
Keyword(s):  
Suicidal Ideation ◽  
Suicidal Behavior ◽  
Tryptophan Hydroxylase ◽  
Association Studies ◽  
Receptor Gene ◽  
Brain Regions ◽  
Depressive Illness ◽  
Control Group ◽  
Serotonergic Activity ◽  
Completed Suicide

Summary: Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of depressive illness and suicidal behavior. Studies have shown that the number of brain and platelet serotonin transporter binding sites are reduced in patients with depression and in suicide victims, and that the density of 5-HT2A receptors is increased in brain regions of depressed in suicide victims and in platelets of depressed suicidal patients. Genes that code for proteins, such as tryptophan hydroxylase, 5-HT transporter, and 5-HT2A receptor, involved in regulating serotonergic neurotransmission, have thus been major candidate genes for association studies of suicide and suicidal behavior. Recent studies by our group and by others have shown that genetic variations in the serotonin-system-related genes might be associated with suicidal ideation and completed suicide. We have shown that the 102 C allele in 5-HT2A receptor gene was significantly associated with suicidal ideation (χ2 = 8.5, p < .005) in depressed patients. Patients with a 102 C/C genotype had a significantly higher mean HAMD item #3 score (indication of suicidal ideation) than T/C or T/T genotype patients. Our results suggest that the 102T/C polymorphism in 5-HT2A receptor gene is primarily associated with suicidal ideation in patients with major depression and not with depression itself. We also found that the 5-HT transporter gene S/L polymorphism was significantly associated with completed suicide. The frequency of the L/L genotype in depressed suicide victims was almost double of that found in control group (48.6% vs. 26.2%). The odds ratio for the L allele was 2.1 (95% CI 1.2-3.7). The association between polymorphism in serotonergic genes and suicidality supports the hypothesis that genetic factors can modulate suicide risk by influencing serotonergic activity.

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