Dataset Information

Nicotinohydrazide.

ABSTRACT: The title mol-ecule (alternative name: pyridine-3-carbohydrazide; C(6)H(7)N(3)O) was obtained from the reaction of ethyl nicotinate with hydrazine hydrate in methanol. In the amide group, the C-N bond is relatively short, suggesting some degree of electronic delocalization in the mol-ecule. The stabilized conformation may be compared with those of isomeric compounds picolinohydrazide (pyridine-2-carbohydrazide) and isonicotinohydrazide (pyridine-4-carbohydrazide). In the title isomer, the pyridine ring forms an angle of 33.79?(9)° with the plane of the non-H atoms of the hydrazide group. This lack of coplanarity between the hydrazide functionality and the pyridine ring is considerably greater than that observed in isonicotinohydrazide (dihedral angle = 17.14°), while picolinohydrazide is almost fully planar. The title isomer forms inter-molecular N-H?O and N-H?N hydrogen bonds, which stabilize the crystal structure.

SUBMITTER: Priebe JP

PROVIDER: S-EPMC2915351 | biostudies-other | 2007

REPOSITORIES: biostudies-other

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Nicotinohydrazide.

Priebe Jacks P JP Mello Renata S RS Nome Faruk F Bortoluzzi Adailton J AJ

Acta crystallographica. Section E, Structure reports online 20071218 Pt 1

The title mol-ecule (alternative name: pyridine-3-carbohydrazide; C(6)H(7)N(3)O) was obtained from the reaction of ethyl nicotinate with hydrazine hydrate in methanol. In the amide group, the C-N bond is relatively short, suggesting some degree of electronic delocalization in the mol-ecule. The stabilized conformation may be compared with those of isomeric compounds picolinohydrazide (pyridine-2-carbohydrazide) and isonicotinohydrazide (pyridine-4-carbohydrazide). In the title isomer, the pyridi ...[more]

PMID: 21200867

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Project description:Rationale: 22q11 deletion syndrome arises from recombination between low copy repeats on chromosome 22. Typical deletions result in hemizygosity for TBX1 associated with congenital cardiovascular disease. Deletions distal to the typically deleted region result in a similar cardiac phenotype but lack extra-cardiac features of the syndrome suggesting that a second haploinsufficient gene maps to this interval. Objective: The transcription factor HIC2 is lost in most distal deletions as well as a minority of typical deletions. We used mouse models to test the hypothesis that HIC2 hemizygosity causes congenital heart disease. Methods and Results: We created a genetrap mouse allele of Hic2. The genetrap reporter was expressed in the heart throughout the key stages of cardiac morphogenesis. Homozygosity for the genetrap allele was embryonic lethal before embryonic day E10.5 while the heterozygous condition exhibited a partially penetrant late lethality. One third of heterozygous embryos had a cardiac phenotype. Magnetic resonance imaging demonstrated a ventricular septal defect with overriding aorta. Conditional targeting indicated a requirement for Hic2 within the Nkx2.5+ and Mesp1+ cardiovascular progenitor lineages but not in the Wnt1+ neural crest or Mef2c+ second heart field lineages. Microarray analysis revealed increased expression of BMP10. Conclusions: Our results demonstrate a novel role for Hic2 in cardiac development. Hic2 is the first gene within the distal 22q11 interval to have a demonstrated haploinsufficient cardiac phenotype in mice. Together our data suggests HIC2 haploinsufficiency likely contributes to the cardiac defects seen in distal 22q11 deletion syndrome. The aim of this microarray experiment was to compare gene expression changes in the E13.5 mouse heart in a conditional knockout of Hic2 (Mesp1Cre/+; Hic2FL/FL) against control. All samples represent pools of isolated hearts from E13.5 mouse embryos. 3 replicates of each genotype were assayed. The genotypes are: 'WT' (Hic2FL/FL) 'KO' (Mesp1Cre/+; Hic2 FL/FL)

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Nicotinohydrazide.

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Nicotinohydrazide.

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