Disease relevance of POU6F1

• Brain 5-HT1A receptor binding in chronic fatigue syndrome measured using positron emission tomography and [11C]WAY-100635 [1].
• The spirodecanone binding in vehicle-treated gerbils subjected to ischemia was unchanged in the brain 5 h after recirculation, compared with that in sham-operated animals [2].
• Critique for: Di Rocco, c.; Di Trapani, G.; Pettorossi, V.E., and Caldarelli, M: On the pathology of experimental hydrocephalus induced by artificial increase in endoventricular CSF pulse pressure. Child's Brain 5: 81--95 (1979) [3].

High impact information on POU6F1

• The authors hypothesized that the variance observed in brain 5-HTR2A binding is genetically mediated, at least in part [4].
• Direct PCR sequencing of the protein coding region failed to reveal changes in the deduced amino acid sequence of the platelet/brain 5-HTT (40,000 base pairs sequence screened), although a conservative single-base substitution representing a silent polymorphism was found [5].
• However, both antibodies substantially reduced the early distribution of nicotine to brain 5 min after a dose [6].
• Brain 5-HT2A receptor occupancy of deramciclane in humans after a single oral administration--a positron emission tomography study [7].
• E max values (% effect induced by 10 muM of 5-HT) for G-protein activation at rat brain 5-HT1A receptors: sarizotan (66.5), bifeprunox (35.9), SSR181507 (25.8), nemonapride (25.7), ziprasidone (20.6), SLV313 (19), aripiprazole (15), tiospirone (8.9) [8].

Chemical compound and disease context of POU6F1

• Intraperitoneal application of vinconate (100 and 300 mg/kg) 10 min and pentobarbital (40 mg/kg) 30 min before ischemia showed a mild reduction in the [3H]CHA binding in the brain 5 h after ischemia [9].

Biological context of POU6F1

• Here we identify novel DNA binding sites for the POU protein mPOU (POU6F1) [10].
• A potential function of Brn-5 may be to suppress the action of proliferative signals in postmitotic neurons and thus prevents them from reentering the cell cycle [11].
• This 5' region was obtained via PCR methods using a human brain 5' RACE-Ready cDNA library [12].
• We also documented seasonal variations in brain serotonergic function by our finding of reduced brain 5-HTT availability in winter (compared to summer) in healthy controls [13].

Associations of POU6F1 with chemical compounds

• Synthesis of a [6-pyridinyl-18F]-labelled fluoro derivative of WAY-100635 as a candidate radioligand for brain 5-HT1A receptor imaging with PET [14].
• The effects of hydrocortisone administration (20 mg, orally, twice daily) on the sensitivity of brain 5-HT1A receptors in healthy volunteers were studied using a buspirone challenge paradigm [15].
• N-(2-(4-(2-Methoxy-phenyl)-1-piperazin-1-yl)ethyl)-N-(2-pyridyl)++ +cyclohexanecarboxamide (WAY-100635), labelled in its amido carbonyl group with 11C (t1/2 = 20.4 min), is a promising radioligand for the study of brain 5-HT1A receptors with positron emission tomography (PET) [16].
• A positron emission tomography study of the effects of treatment with valproate on brain 5-HT2A receptors in acute mania [17].

Other interactions of POU6F1

• Ectopic expression of Brn-5 in dividing NG108-15 cells reduces the level of RNA encoding the proliferating cell nuclear antigen (PCNA) [11].

Analytical, diagnostic and therapeutic context of POU6F1

• We assessed brain 5-HT1A receptor binding potential directly using the specific radioligand [11C]WAY-100635 and positron emission tomography (PET) [1].
• No FBM metabolites were detected in brain 5 min after administration: In silica gel thin-layer chromatography (TLC), a single [14C]FBM peak was detected--Rf = 0.504 (70:30 acetone:hexane) [18].
• This lesion did not demonstrate significant changes in the vasculature but did have radiation necrosis of the surrounding brain 5 years after 25 Gy equivalents of helium-ion radiosurgery [19].

References