mProX™ Human PROK2 Stable Cell Line

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

Prokineticin 2 (Prok2) is a small protein expressed in a subpopulation of neurons in the suprachiasmatic nucleus (SCN), which is the primary circadian pacemaker in mammals. It has been implicated as a candidate output molecule from the SCN to control multiple circadian rhythms. In vivo recording of the circadian calcium rhythm in Prok2 neurons of the SCN has been achieved using Prok2-tTA knock-in mice expressing the tetracycline transactivator specifically in Prok2 neurons. The circadian Ca2+ rhythm in these neurons showed clear rhythms in both light-dark and constant dark conditions, with their peaks around midday. The hours of high Ca2+ coincided with the rest period of the behavioral rhythm, supporting the predicted function of Prok2 neurons in suppressing locomotor activity during both daytime and subjective daytime. Additionally, the application of a hybrid framework called Circadian Gene Regulatory Framework (CGRF) has been introduced to infer circadian gene regulatory relationships from gene expression data. This framework combines the fuzzy C-means clustering algorithm with dynamic time warping distance to efficiently identify gene clusters related to the target gene and determine the significance of genes within a specific cluster. The framework also uses a dynamic vector autoregressive method to analyze selected significant gene expression profiles and reveal directed causal regulatory relationships based on partial correlation. Furthermore, the potential role of Prok2 gene polymorphisms as predictors of methamphetamine use disorder risk and indicators of craving scale in the Chinese Han population has been investigated. The study identified a significant association between the PROK2 gene and both MUD risk susceptibility and craving scale, providing insights into the underlying mechanisms of METH dependence. Lastly, chronic social stress has been shown to blunt core body temperature and molecular rhythms of Rbm3 and Cirbp in the mouse lateral habenula. The study found that chronic social stress dampened temperature amplitudes and fragmented the interdaily stability of temperature rhythms, with recovery observed in stress-resilient mice. The expression of thermosensitive genes Rbm3 and Cirbp in the lateral habenula was also blunted after stress exposure but recovered later.