Dataset Information

Protein identification from a gel band using our MSB-01 service

ABSTRACT: Protein identification from a gel band using our MSB-01 service. This includes in-gel digestion with trypsin, LC-MS/MS, database searching and reporting.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Ixodes Scapularis (black-legged Tick) (deer Tick)

TISSUE(S): Salivary Gland

SUBMITTER: Gary Crispell

LAB HEAD: Gary Crispell

PROVIDER: PXD012827 | Pride | 2019-06-19

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	MSB27237A (F116822).mzid_MSB27237A_(F116822).pride.mgf.gz	Mzid
	MSB27237A (F116822).pride.mztab.gz	Mztab
	MSB27237A.raw	Raw
	MSB27237AF116822.mzid.gz	Mzid
	MSB27237AF116822.mzid_MSB27237A_F116822.MGF	Mzid

Items per page:

1 - 5 of 25

Publications

Discovery of Alpha-Gal-Containing Antigens in North American Tick Species Believed to Induce Red Meat Allergy.

Crispell Gary G Commins Scott P SP Archer-Hartman Stephanie A SA Choudhary Shailesh S Dharmarajan Guha G Azadi Parastoo P Karim Shahid S

Frontiers in immunology 20190517

Development of specific IgE antibodies to the oligosaccharide galactose-α-1, 3-galactose (α-gal) following tick bites has been shown to be the source of red meat allergy. In this study, we investigated the presence of α-gal in four tick species: the lone-star tick (Amblyomma americanum), the Gulf-Coast tick (Amblyomma maculatum), the American dog tick (Dermacentor variabilis), and the black-legged tick (Ixodes scapularis) by using a combination of immunoproteomic appr ...[more]

PMID: 31156631

Similar Datasets

Project description:Cellular senescence due to telomere dysfunction has been hypothesized to play a role in age-associated diseases including idiopathic pulmonary fibrosis (IPF). It has been postulated that paracrine mediators originating from senescent alveolar epithelia signal to surrounding mesenchymal cells and contribute to disease pathogenesis. However, murine models of telomere-induced alveolar epithelial senescence fail to display the canonical senescence-associated secretory phenotype (SASP) that is observed in senescent human cells. In an effort to understand human-specific responses to telomere dysfunction, we modelled telomere dysfunction-induced senescence in a human alveolar epithelial cell line. We hypothesized that this system would enable us to probe for differences in transcriptional and proteomic senescence pathways in vitro and to identify novel secreted protein (secretome) changes that potentially contribute to the pathogenesis of IPF. Following induction of telomere dysfunction, a robust senescence phenotype was observed. RNA-Seq analysis of the senescent cells revealed the SASP and comparisons to previous murine data highlighted species-specific responses to telomere dysfunction. We then conducted a proteomic analysis of the senescent cells using a novel biotin ligase capable of labeling secreted proteins. Candidate biomarkers selected from our transcriptional and secretome data were then evaluated in IPF and control patient plasma. Four novel proteins were found to be differentially expressed between the patient groups: stanniocalcin-1, contactin-1, tenascin C, and total inhibin. Our data show that human telomere-induced, alveolar epithelial senescence results in a transcriptional SASP that is distinct from that seen in analogous murine cells. Our findings suggest that studies in animal models should be carefully validated given the species-specific responses to telomere dysfunction. We also describe a pragmatic approach for the study of the consequences of telomere-induced alveolar epithelial cell senescence in humans.