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Proteome of familial protein S deficiency

ABSTRACT: The plasma samples from four patients with inherited protein S deficiency (PSD, n=4) and three controls with non-protein S deficiency (NPSD, n=3) were collected and subsequently performed on analyses of proteomics.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma

SUBMITTER: Zhuoru He

LAB HEAD: Zhuoru He

PROVIDER: PXD055111 | Pride | 2024-10-17

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Con_P1_680022.raw	Raw
	Con_P3_642762.raw	Raw
	Con_P7_203403.raw	Raw
	PSD_P2_641911.raw	Raw
	PSD_P4_203908.raw	Raw

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1 - 5 of 9

Publications

Proteome and Metabolome Profiling of Anticoagulant Disorders Induced by Familial Protein S Deficiency.

Zhang Caiping C Zhang Yimin Y Liu Binjie B Chen Yongxv Y Xie Yue Y Huang Huiting H Liu Zhongqiu Z He Zhuoru Z

Journal of proteome research 20240912 10

Protein S deficiency (PSD) is an autosomal dominant disorder characterized by congenital thrombophilia. Studies on PSD are limited yet, resulting in a lack of clarity about molecular changes during abnormal coagulation. Proteomics and metabolomics analyses were conducted on the plasma of PSD patients based on liquid and gas chromatography-mass spectrometry (LC- and GC-MS). Differential proteins and metabolites of PSD were then filtered by univariate statistical analysis and subjected to network ...[more]

PMID: 39265992

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Gene expression data from the skin of Cdsniep-/-adult mice

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Gene expression data from the skin of Cdsnep-/- E18.5 embryos

Project description:Peeling Skin Disease (PSD; OMIM 270300) is an inflammatory ichthyosis due to homozygous loss-of-function mutations in Corneodesmosin (CDSN) and characterized by lifelong patchy peeling of the skin associated with eczema, food allergy and severe itching. The pathophysiology of PSD is still poorly known. The initial event of the disease, the detachment of the SC due to a CDSN deficiency, leads to an impairment of the permeability barrier which could in turn trigger erythema, pruritus and atopic manifestations by mechanisms not entirely elucidated. Cdsn-deficient mouse models are interesting tools to decipher these underlying mechanisms. In order to explore the still poorly known pathophysiological mechanisms of PSD, we analyzed the cutaneous transcriptome of two epidermis-specific Cdsn-deficient mouse models representative of early (occurrence of the permeability defect in Cdsnep-/- E18.5 embryos) and chronic (permanent permeability defect in Cdsniep-/- adult mice) phases of the disease We used affymetrix microarrays to explore genes expression in the skin of Cdsnep-/- E18.5 embryos which represent the early phase of the disease.

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