Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels.

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Evaluation of high-fat high-fructose diet treatment in factor VIII (coagulation factor)-deficient mouse model.

P2860

Q52587797-4B35D27D-5754-448F-A807-4BD5BFB9604E

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Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels.

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http://www.wikidata.org/entity/Q41512070

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2017 nî lūn-bûn

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2017年の論文

@ja

2017年論文

@yue

2017年論文

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2017年論文

@zh-hk

2017年論文

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2017年論文

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2017年论文

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2017年论文

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2017年论文

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name

Mice deficient in the anti-hae ...... llebrand factor plasma levels.

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type

Item

label

Mice deficient in the anti-hae ...... llebrand factor plasma levels.

@en

prefLabel

Mice deficient in the anti-hae ...... llebrand factor plasma levels.

@en

P1476

Mice deficient in the anti-hae ...... illebrand factor plasma levels

@en

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Alexandra Grill

http://www.w3.org/2001/XMLSchema#string

Amrit Mann

http://www.w3.org/2001/XMLSchema#string

Avinash Khandagale

http://www.w3.org/2001/XMLSchema#string

Cornelia Karwot

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Davit Manukyan

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Frano Malinarich

http://www.w3.org/2001/XMLSchema#string

Henning Formes

http://www.w3.org/2001/XMLSchema#string

Inge Scharrer

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Kerstin Jurk

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Klytaimnistra Kiouptsi

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P2860

Inversions disrupting the factor VIII gene are a common cause of severe haemophilia A

Mvwf, a dominant modifier of murine von Willebrand factor, results from altered lineage-specific expression of a glycosyltransferase

Sialyltransferase ST3Gal-IV operates as a dominant modifier of hemostasis by concealing asialoglycoprotein receptor ligands.

A conditional knockout mouse model reveals endothelial cells as the principal and possibly exclusive source of plasma factor VIII.

Factor VIII and platelets synergistically accelerate cleavage of von Willebrand factor by ADAMTS13 under fluid shear stress.

Targeting FVIII expression to endothelial cells regenerates a releasable pool of FVIII and restores hemostasis in a mouse model of hemophilia A.

The life cycle of coagulation factor VIII in view of its structure and function.

A monoclonal antibody to von Willebrand factor (vWF) inhibits factor VIII binding. Localization of its antigenic determinant to a nonadecapeptide at the amino terminus of the mature vWF polypeptide.

Systemic blockade of sialylation in mice with a global inhibitor of sialyltransferases.

Joint bleeding in factor VIII deficient mice causes an acute loss of trabecular bone and calcification of joint soft tissues which is prevented with aggressive factor replacement.

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e0183590

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scholarly article

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10.1371/JOURNAL.PONE.0183590

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English

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http://www.w3.org/2001/XMLSchema#string

P478

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Saravanan Subramaniam

Serge C. Thal

Christoph Reinhardt

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2017-08-24T00:00:00Z

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P698

28837614

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P921

hemophilia

Coagulation factor VIII

P932

5570278

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Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels.

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P2860

P2860

Mice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levels.

description

name

type

label

prefLabel

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P921

P932

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P921

P932