Text classification tends to struggle when data is deficient or when it needs to adapt to unseen classes. In such challenging scenarios, recent studies have used meta-learning to simulate the few-shot task, in which new queries are compared to a small support set at the samplewise level. However, this sample-wise comparison may be severely disturbed by the various expressions in the same class. Therefore, we should be able to learn a general representation of each class in the support set and then compare it to new queries. In this paper, we propose a novel Induction Network to learn such a generalized class-wise representation, by innovatively leveraging the dynamic routing algorithm in meta-learning. In this way, we find the model is able to induce and generalize better. We evaluate the proposed model on a well-studied sentiment classification dataset (English) and a real-world dialogue intent classification dataset (Chinese). Experiment results show that on both datasets, the proposed model significantly outperforms the existing state-of-the-art approaches, proving the effectiveness of class-wise generalization in few-shot text classification. * * Corresponding authors: Y.Li and P.Jian.

BTK is a member of the TEC family of non-receptor tyrosine kinases whose deregulation has been implicated in a variety of B-cell-related diseases. We have used structure-based drug design in conjunction with kinome profiling and cellular assays to develop a potent, selective, and irreversible BTK kinase inhibitor, QL47, which covalently modifies Cys481. QL47 inhibits BTK kinase activity with an IC50 of 7 nM, inhibits autophosphorylation of BTK on Tyr223 in cells with an EC50 of 475 nM, and inhibits phosphorylation of a downstream effector PLCγ2 (Tyr759) with an EC50 of 318 nM. In Ramos cells QL47 induces a G1 cell cycle arrest that is associated with pronounced degradation of BTK protein. QL47 inhibits the proliferation of B-cell lymphoma cancer cell lines at submicromolar concentrations.

STK16 is a ubiquitously expressed, myristoylated, and palmitoylated serine/threonine protein kinase with underexplored functions. Recently, it was shown to be involved in cell division but the mechanism remains unclear. Here we found that human STK16 localizes to the Golgi complex throughout the cell cycle and plays important roles in Golgi structure regulation. STK16 knockdown or kinase inhibition disrupts actin polymers and causes fragmented Golgi in cells. In vitro assays show that STK16 directly binds to actin and regulates actin dynamics in a concentration- and kinase activity-dependent way. In addition, STK16 knockdown or kinase inhibition not only delays mitotic entry and prolongs mitosis, but also causes prometaphase and cytokinesis arrest. Therefore, we revealed STK16 as a novel actin binding protein that resides in the Golgi, which regulates actin dynamics to control Golgi structure and participate in cell cycle progression.