Disease relevance of Pou3f1

• It had a sedative effect, with a median toxic dose of 874.8 mg/kg by the Rotorod Toxicity Test at 45 min [1].
• The Mouse Lymphoma Assay (MLA) Workgroup of the International Workshop on Genotoxicity Test Procedures held a second harmonization meeting just prior to the U.S. Environmental Mutagen Society Meeting in New Orleans, LA, in April 2000 [2].
• The identification methods included bile solubility, optochin sensitivity, countercurrent-immunoelectrophoresis (CIEP), and coagglutination (CoA) using laboratory-prepared reagents (LPR) and the Phadebact Pneumococcus Test (Phadebact) [3].
• Meanwhile, in 2002, the OECD Test Guidelines Programme is considering the worldwide acceptance of the validated in vitro phototoxicity and corrosivity tests [4].
• A measure of females' body weight gain revealed that Coc-Test 20 group was significantly higher than other groups particularly during the postpartum phase [5].

Psychiatry related information on Pou3f1

• Both compounds block the hind leg tonic extensor phase of the Maximal Electroshock Seizure (M.E.S.) Test in mice [6].
• Administration of L-Dopa to control mice reduced locomotor and rearing activity throughout the tolerance development period (Test Days 1-12) during the first hour after injection, and then increased locomotor activity during the second hour [7].
• In an object discrimination and reversal learning task in the marmoset, assessed using a Wisconsin General Test Apparatus, ondansetron improved performance in a reversal learning task [8].

High impact information on Pou3f1

• Together these data strongly indicate that Brn-2 function largely overlaps with that of Oct-6 in driving the transition from promyelinating to myelinating Schwann cells [9].
• This suggests that Skn-1a/i and Tst-1 serve redundant functions in epidermis [10].
• Therefore, at least two POU domain genes, Skn-1a/i and Tst-1, serve both distinct and overlapping functions to regulate differentiation of epidermal keratinocytes during normal development and wound healing [10].
• Unexpectedly, the activation of major myelin-specific genes appears to be unaffected by the Tst-1/Oct-6/SCIP mutation, demonstrating that multiple, independently regulated events are required for terminal differentiation of Schwann cells [11].
• In addition, aberrant differentiation and migration of specific neurons in Tst-1/Oct-6/SCIP mutant homozygotes is associated with a fatal breathing defect, providing a model for investigating the regulation of pulmonary homeostasis [11].

Chemical compound and disease context of Pou3f1

• The motor activity reinstatement effect of this dose of L-Dopa upon MPTP-treated mouse behaviour deteriorated from the 13th injection (Test Day 8) of L-Dopa onwards and reached basal level (i.e. no stimulatory effects of the drug) by the 16th administration (Test Day 10) [7].
• In these studies, genistein was evaluated for mutagenicity and clastogenicity in vitro in the S. typhimurium assay (Ames Test), the mouse lymphoma assay and in vivo in the micronucleus test in mice and rats [12].
• Tests which showed good correlation with bioassay results and thus were considered good predictors of tumorigenic potential were: Sustained Epidermal Hyperplasia as measured by epidermal thickness, Nuclear Area of epidermal basal cells, Modified Ames Test and DMSO extraction for PAC content [13].
• To get better insights into the mechanisms of action of these compounds, we studied the effect of local treatment with calcipotriol (vitamin D3 synthetic analogue) and compared it to that of betamethasone dipropionate in a murine contact sensitivity (CS) test, the Mouse Ear Swelling Test. Two haptens were used: oxazolone and paraphenylenediamine [14].

Biological context of Pou3f1

• The class III POU domain protein Brn-1 can fully replace the related Oct-6 during schwann cell development and myelination [15].
• A distal Schwann cell-specific enhancer mediates axonal regulation of the Oct-6 transcription factor during peripheral nerve development and regeneration [16].
• Expression of Oct-6 in HeLa cells is sufficient for transcriptional activation from the octamer motif, identifying Oct-6 as a transcription factor [17].
• The POU domain transcription factor Oct-6 is a major regulator of Schwann cell differentiation and myelination [16].
• We further demonstrate that a tagged version of Oct-6, driven by the SCE, rescues the peripheral nerve phenotype of Oct-6-deficient mice [16].

Anatomical context of Pou3f1

• Expression of the POU domain transcription factor, Oct-6, is attenuated in the adult mouse telencephalon, but increased by neurotoxic damage [18].
• The Oct-6 expression is downregulated upon embryonic stem cell differentiation increasing again during brain development [17].
• Thus, our isolation and characterization of the Oct-6 SCE provides the first description of a cis-acting genetic element that responds to converging signalling pathways to drive myelination in the peripheral nervous system [16].
• The two waves of widespread induction of the Oct-6 gene, one in the primitive ectoderm and another in the primitive brain, both followed by a progressive restriction in the expression patterns suggest a mechanism for the regulation of the gene [19].
• As the anterior neuropore closes, Oct-6 protein is detected in a segment-like pattern in the mid-and forebrain [19].

Associations of Pou3f1 with chemical compounds

• No significant treatment effect was detected by Expanded Disability Status Scale, Nine Hole Peg Test, or number of new gadolinium-enhancing MRI lesions [20].
• The mammalian Scip gene had alanine, glycine, proline, and histidine repeats, but the nonmammalian homologue completely lacked these repeats [21].
• As a consequence, TPA and estrogen activated transcription of the Tst-1/Oct6 gene in a synergistic manner [22].
• Results: Carriers of the MR180V allele showed higher saliva (P < 0.01), plasma cortisol (P < 0.01), and heart rate responses (P < 0.05) to the Trier Social Stress Test than noncarriers (MR180I) [23].
• The results of the Micronucleus Test, an in vivo method, showed that the isolated antimutagenic compound reduced by approximately 68.4% the number of micronucleated polychromatic erythrocytes induced by tetracycline, a known mutagen [24].

Physical interactions of Pou3f1

• The identification of multiple Oct6 binding sites within this fragment suggested that Oct6 directly controls Krox20 transcription [25].
• The myelination-regulating transcription factor Oct6 is involved in a complex modulatory relationship with Ski [26].

Regulatory relationships of Pou3f1

• Although the closely related POU domain protein Brn-2 is coexpressed with Oct-6 in Schwann cells, its loss has only mild consequences [15].

Other interactions of Pou3f1

• Onset and extent of myelination were also indistinguishable from that of the wild type in mice that carried only Brn-1 instead of Oct-6 alleles [15].
• Genetic studies showed that both elements were active in a Krox20 mutant background, while the activity of the MSE, but likely not of the ISE, required the POU domain transcription factor Oct6 at the time of myelination [25].
• Finally, in situ hybridization and transfection analysis suggests that COUP-TFI acts as an upstream regulator of SCIP/Oct-6/Tst-1, a transcription factor involved in axon myelination [27].

Analytical, diagnostic and therapeutic context of Pou3f1

• Sequence analysis of the cDNA encoding the Oct6 protein indicated that the Oct6 gene is a member of the POU-HOMEO domain gene family [28].
• Sample sizes for 85% power to detect a 25% reduction in the 20-minute daytime Murine Multiple Sleep Latency Test require fewer than 20 mice per group for commonly used transgenic background strains [29].
• Quantitative erythropoietin determinations can only be obtained after the examination of both Standard and Test materials in a multiple dose parallel line bioassay with appropriate statistical control [30].
• These experiments were designed to address International Workshop on Genotoxicity Test Procedures validation criteria by evaluating the degree of correspondence between MN-RET measurements generated by flow cytometry (FCM) with those obtained using traditional microscopy-based methods [31].
• Further, results from pulmonary function tests performed on the same allergic animals indicated that only animals from Test I and Test II groups had impaired lung function after allergen challenge [32].

References