Dataset Information

Pulldown GST-SH3 domains of Endophilin and rat brain lysates

ABSTRACT: Pulldown experiments using GST-SH3 domains from hman Endophilin A1, A2 and A3 and rat brain lysates

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

SUBMITTER: Emmanuel Boucrot

LAB HEAD: Emmanuel Boucrot

PROVIDER: PXD010090 | Pride | 2018-08-06

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	(F013770).mzid.gz_(F013770).pride.mgf.gz	Mzid
	(F013770).pride.mztab.gz	Mztab
	(F013771).mzid.gz_(F013771).pride.mgf.gz	Mzid
	(F013771).pride.mztab.gz	Mztab
	(F013772).mzid.gz_(F013772).pride.mgf.gz	Mzid

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Publications

FBP17 and CIP4 recruit SHIP2 and lamellipodin to prime the plasma membrane for fast endophilin-mediated endocytosis.

Chan Wah Hak Laura L Khan Shaheen S Di Meglio Ilaria I Law Ah-Lai AL Lucken-Ardjomande Häsler Safa S Quintaneiro Leonor M LM Ferreira Antonio P A APA Krause Matthias M McMahon Harvey T HT Boucrot Emmanuel E

Nature cell biology 20180730 9

Endocytosis mediates the cellular uptake of micronutrients and the turnover of plasma membrane proteins. Clathrin-mediated endocytosis is the major uptake pathway in resting cells1, but several clathrin-independent endocytic routes exist in parallel2,3. One such pathway, fast endophilin-mediated endocytosis (FEME), is not constitutive but triggered upon activation of certain receptors, including the β1 adrenergic receptor4. FEME activates promptly foll ...[more]

PMID: 30061681

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Project description:The glutathione S-transferase (GST) gene family codes for enzymes that detoxify xenobiotics by catalyzing the conjugation of xenobiotics to glutathione. Based on reports that inherited copy number variations (CNV) in the genome modulate some GST expression levels and with the knowledge that cigarette smoke contains >3000 xenobiotics, and that the small airway epithelium and alveolar macrophages are involved early in the pathogensis of smoking-induced lung disease, we asked: do germline CNVs modulate GST expression level in the small airway epithelium and alveolar macrophages? Affymetrix HG U133 Plus 2.0 microarrays were used to survey GST gene expression in the small airway epithelium and alveolar macrophages obtained by bronchoscopic brushings from current smokers (n=35) and nonsmokers (n=35). The CNV genotypes of these 70 subjects were determined by Affymetrix Human SNP array 5.0 chips. Sixteen % of subjects had deletions of both GSTM1 alleles. These deletions were associated with reduced GSTM1 mRNA levels in both the small airway epithelium (p<10-7) and alveolar macrophages (p<0.05). Thirty % of subjects had homozygous deletions of GSTT1 with concomitant reduced mRNA levels in both small airway epithelium and alveolar macrophages (p<10-7). In contrast, genes flanking the CNV regions of both GST genes showed no difference in expression level among subjects with and without the GST deletions (p>0.3). Interestingly, GSTT2B, a duplicate gene of GSTT2, exhibited homozygous deletion in blood in 27% of subjects and was not expressed in small airway epithelium in the remainder of subjects but was expressed in alveolar macrophages of heterozygotes and wild type subjects, proportionate to genotype (p<10-3). These data demonstrate that highly prevalent CNV deletions of genes critical to ameliorating smoking-associated xenobiotic-induced damage in the lung can result in significant modulation of the gene expression levels, with the linear relationship of genotype to expression level suggesting minimal compensation of gene expression levels in heterozygotes consistent with GST polymorphisms playing a role in the risk for development of smoking-induced lung disease.