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Abstract: Neurofibromatosis type 1 (NF1) microdeletion is a large genomic deletion that embraces at least 11 continuous genes at human chromosome 17q11.2. To date, most of these genes’ functions still remain undefined. In this study, we report an unknown cytokine receptor like molecule (p48.2) that is frequently deleted in patients with type-1 and type-2 NF1 microdeletions in the neurofibromin locus. The cloned gene has 1317 base pair long that encodes a 438aa intracellular protein. The gene was subsequently named p48.2 based on its predicted molecular weight. A typical fibronectin type III (FNIII) domain was identified in p48.2 between Arg176 and Pro261 in which a palindromic Arg-Gly-Asp (RGD) repeat plus a putative Trp-Ser-X-Trp-Ser (WSXWS) motif were found at the domain''s C-terminus. p48.2 mRNAs were abundant in many tumor cell lines and normal human tissues and up-regulated in some freshly isolated lung cancer and leukemia cells. Interestingly, over-expression of p48.2 in human embryo kidney 293T cells could significantly cause G0/G1 arrest and prevented S phase entry. In contrast, repressing endogenous p48.2 gene expression by specific siRNA markedly reduced G0/G1 population. Importantly, over-expression of p48.2 could significantly up-regulate rather than down-regulate cyclin D1 and cyclin D3 expressions. We further showed that the induction of cyclin D1 expression was directly due to the activation of signal transducers and activators of transcription 3 (STAT3), but was independent of RAS/mitogen-activated protein kinase (RAS/MAPK) signaling pathway. Thus, p48.2 may represent a novel type of intracellular protein functioning as a negative regulator at the G0/G1 phase. [Copyright &y& Elsevier]

• Applying the essential oils into the prevention of Panax notoginseng disease. • Combination of essential oils with chemical pesticide to avoid environmental pollution and pesticide resistance problems. • The possible action mechanisms of essential oils to the pathogen. • Providing some basis for essential oils to be used as natural alternatives to commercial fungicides. In order to control the occurrence of Panax notoginseng (Burk.) F.H. Chen diseases, the antifungal effects and action mechanism of essential oils (EOs) against the pathogenic fungi were investigated. The antifungal effect of Mentha haplocalyx Briq. and Schizonepeta tenuifolia Briq. essential oils (EOs) were determined in vivo and in vitro to develop green fungicides to eradicate fungi pathogens affecting Panax notoginseng. The inhibition rates of M. haplocalyx and S. tenuifolia EOs (50 mg/mL) on Fusarium oxysporum , Fusarium solani , Cylindrocarpon destructans , Pythium aphanidermatum , Botrytis cinerea , Colletotrichum gloeosporioides and Rhizoctonia solani reached 100.00 % and were assessed by the Oxford cup method. The chemical constituents of M. haplocalyx and S. tenuifolia EOs were analyzed by GC–MS. Low MIC values of M. haplocalyx EO, S. tenuifolia EO and its main components against six fungal strains from P. notoginseng were found, which indicated all have substantial antifungal activity. Furthermore, synergistic effects between the EOs and the agrochemical hymexazol against P. notoginseng pathogens were observed. F. oxysporum was chosen as dominant fungi pathogen to investigate the mechanism of action of M. haplocalyx EO. The antifungal effect of M. haplocalyx EO on F. oxysporum in vitro was investigated. The high M. haplocalyx EO concentrations inhibited the spore germination rates, mycelia dry weights and spore yields and disturbed the mycelia soluble protein and reducing sugar contents; it also increased the cell membrane permeability. M. haplocalyx EO also induced decreased SDH and NADH oxidase activities and caused extreme alterations in ultrastructures compared with the control. Altogether, the antifungal mechanism of M. haplocalyx EO may seemed to consist in penetrating and dissolving the mitochondrial membranes. Overall, M. haplocalyx EO and its major compounds show potential to be used as natural alternatives to commercial fungicides for controlling F. oxysporum infection of P. notoginseng. [ABSTRACT FROM AUTHOR]