In the test session, there was no difference between KO and wild-type males (Fig. species 7, 8. P11 consists of two EF-hands separated by a central small region, and the EF-hand at the C-terminal is vital for its target binding 9-12. Unlike other members, P11 is Ca2+ insensitive because of essential amino acid replacements in its EF-hand Ca2+-binding loops that keep the protein in a permanently active status 13, 14. P11 is expressed ubiquitously 15, 16, especially in brain regions that are implicated in the pathophysiology of depression, including the nucleus accumbens, cerebral cortex, prelimbic cortex and hippocampus17-22. P11 usually exists in the form of annexin II-P11 heterotetramer (AIIt) 23, 24. P11 plays important roles in depression together with several neurotransmitter receptors, such as 5-hydroxytryptamine (5-HT1B) receptor, 5-HT4 receptor and metabotropic glutamate receptor 5 (mGluR5) 25-29. Recent studies indicated that P11 plays roles in both depression and Parkinson’s disease 30-32. In addition, P11 contributes to the clinical hemorrhagic phenotypes of acute promyelocytic leukemia as a plasminogen receptor 33. Dysregulation of P11 was also involved in cancers 34, 35, fatty livers 36, cocaine reward and cannabis dependence 37, 38, and Diarrhea-predominant Irritable Bowel Syndrome 39. These studies suggested that P11 is multifunctional Tiglyl carnitine in regulation of development of various diseases in humans, in addition to its major roles in depression. Neurogenesis was first detected in the dentate gyrus of young rats by injection with thymidine-H3 Tiglyl carnitine 40. In humans, adult neurogenesis even persisted into the eighth decade of life, although quiescent stem cell pools and angiogenesis declined 41. However, another study showed that the number of proliferating progenitors and young neurons in the dentate gyrus decreased sharply after birth and neurogenesis were scarcely observed in teenagers 42. In adult humans, many questions concerning neurogenesis in hippocampus remain unanswered 43, particularly, evolutionary divergence in brain exists between humans and rodents. Treatment of antidepressant agent fluoxetine can increase cell proliferation in hippocampus of wild-type Tiglyl carnitine mice. However, no difference between fluoxetine-treated and control KO mice was observed 44, indicating an association of P11 with cell proliferation. Although roles of P11 in many activities and processes have been well documented, a direct and precise function for P11 in cell proliferation and its possible contribution to psychological disorders remain elusive. To explore the functions of P11 in cell proliferation and its potential contribution to depression, memory deficit and anxiety, in this study, we generated knockout mice, as well as knockout MEF cell lines, using CRISPR/Cas9 technology. By comparing cell proliferation of leads to a decreased cell proliferation. Moreover, knockout resulted in a larger cell size, compared with that of wild type, which resulted probably from accumulated F-actin stress fibers. Moreover, BrdU staining in the Tiglyl carnitine hippocampus showed a decrease in the number of proliferating cells in KO mice. Then we observed anxiety-like disorder in addition to Colec10 depression-like phenotype in knockout mice. Besides, knockout of P11 led to memory deficit in female mice, while not in males. These findings are valuable for understanding of the roles of P11 in the neurological disorders. Materials and Tiglyl carnitine methods Animals C57BL/6 wild-type mice were purchased from Wuhan University Center for Animal Experiment (Wuhan, China) and Shanghai Biomodel Organism Science & Technology Development (Shanghai, China). All animal experiments and methods were performed in accordance.