This a model from the article:
Limit cycle models for circadian rhythms based on transcriptional regulation in Drosophila and Neurospora.
Leloup JC, Gonze D, Goldbeter A. J Biol Rhythms.1999 Dec;14(6):433-48. 10643740,
Abstract:
We examine theoretical models for circadian oscillations based on transcriptional regulation in Drosophila and Neurospora. For Drosophila, the molecular model is based on the negative feedback exerted on the expression of the per and tim genes by the complex formed between the PER and TIM proteins. For Neurospora, similarly, the model relies on the feedback exerted on the expression of the frq gene by its protein product FRQ. In both models, sustained rhythmic variations in protein and mRNA levels occur in continuous darkness, in the form of limit cycle oscillations. The effect of light on circadian rhythms is taken into account in the models by considering that it triggers degradation of the TIM protein in Drosophila, and frq transcription in Neurospora. When incorporating the control exerted by light at the molecular level, we show that the models can account for the entrainment of circadian rhythms by light-dark cycles and for the damping of the oscillations in constant light, though such damping occurs more readily in the Drosophila model. The models account for the phase shifts induced by light pulses and allow the construction of phase response curves. These compare well with experimental results obtained in Drosophila. The model for Drosophila shows that when applied at the appropriate phase, light pulses of appropriate duration and magnitude can permanently or transiently suppress circadian rhythmicity. We investigate the effects of the magnitude of light-induced changes on oscillatory behavior. Finally, we discuss the common and distinctive features of circadian oscillations in the two organisms.

This particular version of the model has been translated from equations 4a-4c (Neurospora).

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Leloup JC, Gonze D, Goldbeter A. (1999) - version02
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute

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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novere N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

LloydCatherinec.lloyd@auckland.ac.nzUniversity of AucklandChelliahVijayalakshmiviji@ebi.ac.ukEMBL-EBI2011-01-14T14:22:45Z2011-01-18T12:23:47Z t offset amplitude phase pulseDuration cyclePeriod rampDuration offset 0.5 amplitude 1 cyclePeriod t phase cyclePeriod t phase cyclePeriod rampDuration 0.5 amplitude 1 cyclePeriod t phase cyclePeriod t phase cyclePeriod pulseDuration rampDuration 0.5 amplitude 1 cyclePeriod t phase cyclePeriod t phase cyclePeriod cyclePeriod rampDuration vs KI n KI n FN n vm M Km M ks M k2 FN vd FC Kd FC k1 FC k1 FC k2 FN FC FN step1 stepFunction t offsetStep1 amplitudeStep1 phaseStep1 pulseDurationStep1 cyclePeriodStep1 rampDurationStep1 t 72 4