CLEC-2 contributes to hemostasis independently of classical hemITAM signaling in mice.

scientific article published on 23 August 2017

CLEC-2 contributes to hemostasis independently of classical hemITAM signaling in mice. is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1182/BLOOD-2017-03-771907
P698PubMed publication ID28835437

P50authorSteve P. WatsonQ37383398
David StegnerQ37829231
Elizabeth J HainingQ63409979
Bernhard NieswandtQ88838569
P2093author name stringJohannes A Eble
Deya Cherpokova
Sarah Beck
Karen Wolf
Isabelle C Becker
P433issue20
P407language of work or nameEnglishQ1860
P304page(s)2224-2228
P577publication date2017-08-23
P1433published inBloodQ885070
P1476titleCLEC-2 contributes to hemostasis independently of classical hemITAM signaling in mice
P478volume130

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cites work (P2860)
Q90454274C-type lectin receptors of the Dectin-1 cluster: Physiological roles and involvement in disease
Q88182685C-type lectins in immunity and homeostasis
Q58761586Cobalt hematoporphyrin inhibits CLEC-2-podoplanin interaction, tumor metastasis, and arterial/venous thrombosis in mice
Q92857675Early Host Interactions That Drive the Dysregulated Response in Sepsis
Q98186915Expression of DC-SIGN-Like C-Type Lectin Receptors in Salmo salar
Q55325579Flexible Signaling of Myeloid C-Type Lectin Receptors in Immunity and Inflammation.
Q46004241Platelet CLEC-2: a molecule with 2 faces.
Q87817429Platelets at the Vascular Interface
Q91106197Snake venom rhodocytin induces plasma extravasation via toxin-mediated interactions between platelets and mast cells
Q59335689The Platelet Response to Tissue Injury

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