The purification, crystallization and preliminary structural characterization of human MAWDBP, a member of the phenazine biosynthesis-like protein family

Herde, Petra; Blankenfeldt, Wulf

doi:10.1107/s1744309106015648

Cited by 2 publications

(4 citation statements)

References 22 publications

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“…The functions of the identified proteins seemed quite diverse, but we were able to deduce a candidate of the protein cluster from the overall analysis of signaling pathways and references. The regulatory mechanisms of 11 proteins identified in this study was reported by previous investigations, including Cdc42, vimentin, annexinA2, HSP90B1, LSP1, , GRP78, and cathepsin D that were up-regulated in UC, and HSF2, galectin-3, VDAC-1and MAWBP which were down-regulated. Interestingly, these 11 proteins were all involved in P38 MAPK pathway directly or indirectly.…”

Section: Resultssupporting

confidence: 83%

“…Furthermore, MAWBP, which was down-regulated in UC group, was first identified as a binding partner of hMAWD “putative human mitogen-activated protein kinase (MAPK) activator with WD repeats”. It is a WD-40 repeat-containing β-propeller protein believed to participate in an MAPK signaling pathway . Hence, we included it into the differential protein cluster due to its possible involvement of signal transduction of P38 MAPK pathway.…”

Section: Resultsmentioning

confidence: 99%

“…It is a WD-40 repeat-containing β-propeller protein believed to participate in an MAPK signaling pathway. 22 Hence, we included it into the differential protein cluster due to its possible involvement of signal transduction of P38 MAPK pathway. Together, our data suggest that activation of P38 MAPK pathway is elevated in UC.…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of P38 MAPK Pathway as a Molecular Signature in Ulcerative Colitis

Zhao

Kang

et al. 2011

J. Proteome Res.

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Early diagnosis and treatment of ulcerative colitis (UC) is clinically challenging. To overcome this problem, we explored the interrelated multiplex signaling pathway to identify molecular signatures in UC by using integrated strategy in proteomics. Intestinal mucosa of 12 UC cases and 12 normal controls underwent comparative proteomic analysis. A total of 26 unique differential proteins were identified, including 12 up-regulated and 14 down-regulated in UC group. A differential protein cluster, consisting of 11 proteins involved in p38 mitogen-activated protein kinase (MAPK) pathway, was deduced and validated by Western blot. Furthermore, three proteins elicited from the protein cluster, phosphorylated p38, MAWBP and galectin-3, as a molecular signature, were analyzed by immunohistochemistry on 118 UC and normal samples. Increased expression of P-p38 and down-regulated MAWBP and/or galectin-3 were detected in UC compared to normal samples (p < 0.001). This signature correlated with disease progression of UC (p < 0.01), and classified UC risk with high sensitivity (94.83 ± 2.91%) and specificity (98.33 ± 1.65%). In addition, P38 MAPK pathway modulated the expression of the protein clusters in macrophage cell line as evidenced by the alteration with specific inhibitor SB203580. These results indicate that molecular signature of P38 MAPK pathway might be a potential biomarker for evaluating UC risk.

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Section: Resultssupporting

confidence: 83%

Section: Resultsmentioning

confidence: 99%

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Evaluation of P38 MAPK Pathway as a Molecular Signature in Ulcerative Colitis

Zhao

Kang

et al. 2011

J. Proteome Res.

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“…However, the exact molecular function of MAWDBP is still unknown. A recent report has described increased levels of MAWDBP mRNA or protein in insulin resistance [76]. Although no reports are available regarding a clear mechanism from this data alone, it is possible to relate this protein to a role in insulin signal transduction and hence, insulin resistance [77].…”

Section: Proteomics Studymentioning

confidence: 91%

Proteomic and transcriptomic analysis for streptozotocin‐induced diabetic rat pancreas in response to fungal polysaccharide treatments

et al. 2008

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In an attempt to search for novel biomarkers for monitoring diabetes prognosis, we examined the influence of the hypoglycemic fungal extracellular polysaccharides (EPS) on the differential change in pancreatic proteome and transcriptome in streptozotocin (STZ)-induced diabetic rats using 2-DE-based protein mapping and oligonucleotide microarray analysis. The 2-DE system separated more than 2000 individual spots, demonstrating that 34 proteins out of about 500 matched spots were differentially expressed. A total of 22 overexpressed and 12 underexpressed proteins in 2-DE map were observed (p<0.05) between the healthy and diabetic rats, of which 26 spots were identified by PMF analysis. Of these, significant down regulation of carbonyl reductase (Cbr), hydroxymethylglutaryl-CoA synthase (HMGCS), and putative human mitogen-activated protein kinase activator with WD repeats-binding protein (MAWDBP) in diabetic pancreas were reported for the first time in this study. When treated with EPS, all these four proteins were reverted to normal levels. The microarray analysis revealed that 96 out of 1272 genes were down- or up-regulated in the diabetic rats and the altered transcript levels of many of these genes were reversed after EPS treatment. In particular, ROS generation in rat islets was significantly increased after STZ treatment, thereafter EPS treatment was likely to play a preventive role in beta-cell destruction mediated by STZ. Taken together, EPS may act as a potent regulator of gene expression for a wide variety of genes in diabetic rats, particularly in antioxidative stress, insulin biosynthesis, and cell proliferation.

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The purification, crystallization and preliminary structural characterization of human MAWDBP, a member of the phenazine biosynthesis-like protein family

Cited by 2 publications

References 22 publications

Evaluation of P38 MAPK Pathway as a Molecular Signature in Ulcerative Colitis

Evaluation of P38 MAPK Pathway as a Molecular Signature in Ulcerative Colitis

Proteomic and transcriptomic analysis for streptozotocin‐induced diabetic rat pancreas in response to fungal polysaccharide treatments

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