Dataset Information

Identification of splicing legumain from Momordica cochinchinesis

ABSTRACT: Analyzse the seed extract of Momordica cochinchinesis displaying legumain activity to identify the coeluted lectin by MALDI-TOF MS/MS

INSTRUMENT(S): TOF/TOF 5800

ORGANISM(S): Momordica Cochinchinensis

TISSUE(S): Seed

SUBMITTER: Xinya Hemu

LAB HEAD: James P. Tam

PROVIDER: PXD028325 | Pride | 2022-02-15

REPOSITORIES: Pride

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Publications

The legumain McPAL1 from Momordica cochinchinensis is a highly stable Asx-specific splicing enzyme.

Liew Heng Tai HT To Janet J Zhang Xiaohong X Hemu Xinya X Chan Ning-Yu NY Serra Aida A Sze Siu Kwan SK Liu Chuan-Fa CF Tam James P JP

The Journal of biological chemistry 20211026 6

Legumains, also known as asparaginyl endopeptidases (AEPs), cleave peptide bonds after Asn/Asp (Asx) residues. In plants, certain legumains also have ligase activity that catalyzes biosynthesis of Asx-containing cyclic peptides. An example is the biosynthesis of MCoTI-I/II, a squash family-derived cyclic trypsin inhibitor, which involves splicing to remove the N-terminal prodomain and then N-to-C-terminal cyclization of the mature domain. To identify plant legumains responsible for the maturatio ...[more]

PMID: 34710371

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Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. In response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expression (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in histone variant H2A.Z occupancy associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed H2A.Z ChIP-Seq in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Please note that RNA-seq data generated in conjunction to this ChIP-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5628 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5628 ).

			Action	DRS
	F062367.csv	Csv
	F062367.dat	Other
	H1_MSMS_1357.5000_15.t2d	Other
	H1_MSMS_1538.0000_12.t2d	Other
	H1_MSMS_1628.0000_10.t2d	Other