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RGS10L phosphorylation site determination Bottom-Up

ABSTRACT: RGS10L phosphorylatin site was determined. Trypsin is not good for generating a peptide containing the potential site, and the initial study was done using the intact protein. From the Top-Down study, the phosphorylatin site of the A->S variant was ambiguous. The firnal confirmation was done using AspN digest.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Escherichia Coli Mus Musculus (mouse)

SUBMITTER: Motoshi Suzuki

LAB HEAD: Kirk M. Druey

PROVIDER: PXD023753 | Pride | 2021-11-03

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	PI20-24854-A171SKDC20-L3.msf	Msf
	PI20-24854-A171SKDC20-L3.mzML	Mzml
	PI20-24854-A171SKDC20-L3.mzid.gz	Mzid
	PI20-24854-A171SKDC20-L3.pdResult	Other
	PI20-24854-A171SKDC20-L3.raw	Raw

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Publications

Short stature and combined immunodeficiency associated with mutations in RGS10.

Chinn Ivan K IK Xie Zhihui Z Chan Eunice C EC Nagata Bianca M BM Koval Alexey A Chen Wei-Sheng WS Zhang Fan F Ganesan Sundar S Hong Diana N DN Suzuki Motoshi M Nardone Glenn G Moore Ian N IN Katanaev Vladimir L VL Balazs Andrea E AE Liu Chengyu C Lupski James R JR Orange Jordan S JS Druey Kirk M KM

Science signaling 20210727 693

We report the clinical and molecular phenotype of three siblings from one family, who presented with short stature and immunodeficiency and carried uncharacterized variants in <i>RGS10</i> (c.489_491del:p.E163del and c.G511T:p.A171S). This gene encodes regulator of G protein signaling 10 (RGS10), a member of a large family of GTPase-activating proteins (GAPs) that targets heterotrimeric G proteins to constrain the activity of G protein-coupled receptors, including receptors for chemoattractants. ...[more]

PMID: 34315806

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RGS10L phosphorylation site determination Top-Down

Project description:The phosphorylation sites of 4 recombinant RGS10L variants were determined using Top-Down study.

2021-11-03 | PXD023752 | Pride

Proteomics Using Proteases Alternative to Trypsin Benefits from Sequential Digestion with Trypsin

Project description:High specificity and ease of use make trypsin the most used enzyme in proteomics. Proteases with complementary cleavage specificity to trypsin have been applied to obtain additional data. However, use of proteases with broad specificity proved especially challenging. In this work, we analyzed the characteristics of five protease alternatives to trypsin for protein identification and sequence coverage when applied to S. pombe whole cell lysates. The specificity of the protease heavily impacted on the number of proteins identified. Proteases with higher specificity let to the identification of more proteins than proteases with lower specificity. However, AspN, GluC, chymotrypsin and proteinase K largely benefited from being paired with trypsin in sequential digestion, as had been shown by us for elastase before. In the most extreme case, the addition of trypsin to a proteinase K digest increased the number of identified proteins by 524 %. Also, AspN (82 %) and GluC (74 %) protein identifications largely improved following the additional digestion with trypsin. In general, protein identifications improved most over the use of the single protease when the enzymes followed on an initial digestion with trypsin. In the most extreme case, the sequential digest with trypsin and AspN yielded even higher number of protein identifications than digesting with trypsin alone.

2021-06-07 | PXD017321 | Pride

Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs [mouse]

Project description:Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs

2020-04-13 | GSE109642 | GEO

Characterization of WN NS3 and AspN proteases

Project description:Characterization of WN NS3 protease and characterization of AspN protease with double digestion protocol

2021-02-04 | PXD022973 | Pride

Proteomic and phosphoproteomic analyses of protein PKA catalytic-alpha-null mpkCCD cells and PKA catalytic-beta-null mpkCCD cells.

Project description:Protein Kinase A (PKA) is a widely studied protein that has been viewed by most investigators as a single entity, although its catalytic subunits are coded in the genome by two separate genes, PKA catalytic alpha (Gene symbol: Prkaca) and PKA catalytic beta Gene symbol: Prkacb). At an amino-acid level, the two are 91.5 percent identical and the catalytic domains are virtually identical. (Footnote: A third entity PKA catalytic gamma, is not widely expressed and will not be considered here.) We have recently succeeded in using CRISPR-Cas9 to create disruptive mutations in both PKA genes (PKA double KO, or PKA dKO) in vasopressin-responsive kidney epithelial cells (mpkCCD cells). Here we carry out mass spectrometry based quantitative proteomics and phosphoproteomics separately in PKA catalytic-alpha and PKA catalytic-beta single knockouts address the issue of function difference between these two PKA catalytic subunits.

2020-06-01 | PXD015050 | Pride

The regulatory landscape of the human HPF1- and ARH3-dependent ADP-ribosylome (part 2)

Project description:Despite the involvement of Poly(ADP-ribose) polymerase-1 (PARP1) in many important biological pathways, the target residues of PARP1-mediated ADP-ribosylation remain ambiguous. To explicate the ADP-ribosylation regulome, we analyze human cells depleted for key regulators of PARP1 activity, histone PARylation factor 1 (HPF1) and ADPribosylhydrolase 3 (ARH3). Using quantitative proteomics, we characterize 1,596 ADP-ribosylation sites, displaying up to 1000-fold regulation across the investigated knockout cells. We find that HPF1 and ARH3 inversely and homogenously regulate the serine ADP-ribosylome on a proteome-wide scale with consistent adherence to lysine-serine-motifs, suggesting that targeting is independent of HPF1 and ARH3. Notably, we do not detect an HPF1-dependent target residue switch from serine to glutamate/aspartate under the investigated conditions. Our data support the notion that serine ADP-ribosylation mainly exists as mono-ADP-ribosylation in cells, and reveal a remarkable degree of histone co-modification with serine ADP-ribosylation and other post-translational modifications.

2021-10-11 | PXD027504 | Pride

Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs [mouse]

Project description:Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs [mouse]

| PRJNA431587 | ENA

Towards comprehensive plasma proteomics by orthogonal protease digestion

Project description:Rapid and consistent protein identification across large clinical cohorts is an important goal for clinical proteomics. With the development of data-independent technologies (DIA/SWATH-MS), it is now possible to analyze hundreds of samples with great reproducibility and quantitative accuracy. However, this technology benefits from empirically derived spectral libraries that define the detectable set of peptides and proteins. Here we apply a simple and accessible tip-based workflow for the generation of spectral libraries to provide a comprehensive overview on the plasma proteome in individuals with and without active tuberculosis (TB). To boost protein coverage, we utilized non-conventional proteases such as GluC and AspN together with the gold standard trypsin, identifying more than 30,000 peptides mapping to 3,309 proteins. Application of this library to quantify plasma proteome differences in TB infection recovered more than 400 proteins in 50 minutes of MS-acquisition, including diagnostic Mycobacterium Tuberculosis(Mtb) proteins that have previously been detectable primarily by antibody-based assays and intracellular proteins not previously described to be in plasma.

2021-07-29 | PXD025671 | Pride

Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs, and PC-3 cells exposed to conditioned media +/- ASPN variants

Project description:Gene expression analysis of Aspn+/+ and Aspn-/- fetal MSCs, and PC-3 cells exposed to conditioned media +/- ASPN variants

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Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

2014-04-01 | E-GEOD-48815 | biostudies-arrayexpress

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