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celosia argentea/nikotin
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Molecular cloning and functional identification of a ribosome inactivating/antiviral protein from leaves of post-flowering stage of Celosia cristata and its expression in E. coli.
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A full-length cDNA clone, encoding a ribosome inactivating/antiviral protein (RIP/AVP) was isolated from the cDNA library of post-flowering stage of Celosia cristata leaves. The full-length cDNA consisted of 1015 nucleotides, with an open reading frame encoding 283 amino acids. The deduced amino
Purification of a ribosome-inactivating protein with antioxidation and root developer potencies from Celosia plumosa.
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Considering Celosia plumosa as a potent antiviral plant, the attempt was made to determine, purify and characterize its proteinaceous antiviral elements against tobacco mosaic virus hypersensitive response on Nicotiana glutinosa. By using 60% ammonium sulphate-precipitation, FPLC-based
Heterologous expression of stress-responsive DUF538 domain containing protein and its morpho-biochemical consequences.
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As a usual response, plants induce/activate various proteins which are thought to be involved in defense mechanisms against the biotic and abiotic stresses they may be confronted with. The novel DUF538 domain containing proteins with unknown functions have been found to be induced/activated in
Complementation analysis of triple gene block of Potato virus S (PVS) revealed its capability to support systemic infection and aphid transmissibility of recombinant Potato virus X.
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Triple gene block (TGB) sequences derived from isolates of ordinary Potato virus S (PVS-O) and Chenopodium-systemic (PVS-CS) were analyzed. Although the TGB sequences did not reveal any specific difference within the 7K protein, some specific differences within the 25K and 12K ORFs were found. In
A New Natural Host of Lisianthus necrosis virus in Taiwan.
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Lisianthus necrosis virus (LNV) was first identified as a fungus-borne virus that induced systemic necrosis in lisianthus (Eustoma russellianum) in Japan (2). In Taiwan, LNV causes systemic bright yellow chlorosis followed by necrosis in lisianthus (1). The disease was able to spread through the
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