Dataset Information

U. Minnesota / Medical College of Wisconsin - Gihan Gunaratne

ABSTRACT: Protein identification from a gel band. This includes in-gel digestion with trypsin, LC-MS/MS, data analysis and reporting.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Gihan Gunaratne

LAB HEAD: Jonathan Marchant

PROVIDER: PXD024153 | Pride | 2022-02-16

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	MSB47061A.raw	Raw
	MSB47061A__F162378_.mzid.gz	Mzid
	MSB47061A__F162378_.mzid_MSB47061A__F162378_.MGF	Mzid
	MSB47062A.raw	Raw
	MSB47062A__F162379_.mzid.gz	Mzid

Items per page:

1 - 5 of 30

Publications

Essential requirement for JPT2 in NAADP-evoked Ca<sup>2+</sup> signaling.

Gunaratne Gihan S GS Brailoiu Eugen E He Shijun S Unterwald Ellen M EM Patel Sandip S Slama James T JT Walseth Timothy F TF Marchant Jonathan S JS

Science signaling 20210323 675

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that releases Ca<sup>2+</sup> from acidic organelles through the activation of two-pore channels (TPCs) to regulate endolysosomal trafficking events. NAADP action is mediated by NAADP-binding protein(s) of unknown identity that confer NAADP sensitivity to TPCs. Here, we used a "clickable" NAADP-based photoprobe to isolate human NAADP-binding proteins and identified Jupiter microtubule-associated homolog 2 (JPT2) as a TPC ...[more]

PMID: 33758061

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.