Results 51 to 60 of about 24,575,655 (169)

CLEC‐2 is not required for platelet aggregation at arteriolar shear [PDF]

open access: yesJournal of Thrombosis and Haemostasis, 2010
The C-type lectin receptor CLEC-2 is expressed primarily on the surface of platelets, where it is present as a dimer, and is found at low level on a subpopulation of other hematopoietic cells, including mouse neutrophils [1–4] Clustering of CLEC-2 by the snake venom toxin rhodocytin, specific antibodies or its endogenous ligand, podoplanin, elicits ...
Craig E, Hughes   +5 more
openaire   +2 more sources

CLEC-2 is required for development and maintenance of lymph nodes [PDF]

open access: yesBlood, 2014
Key Points CLEC-2 is necessary for lymphatic cell proliferation and lymph node anlage persistence after birth. Lack of CLEC-2 expression on megakaryocytes and platelets compromises lymph node integrity in adult life.
Cécile, Bénézech   +10 more
openaire   +2 more sources

The novel platelet activation receptor CLEC-2

open access: yesPlatelets, 2011
The c-type lectin-like receptor 2 (CLEC-2) was first identified from a bio-informatic screen for c-type lectin-like receptors. However, neither its function nor its ligand(s) had been elucidated for several years. In 2006, we reported that the receptor is expressed on the surface of platelets and serves as a receptor for the snake venom rhodocytin ...
Katsue, Suzuki-Inoue   +2 more
openaire   +2 more sources

Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2

open access: yesRetrovirology, 2010
Background Platelets are associated with HIV in the blood of infected individuals and might modulate viral dissemination, particularly if the virus is directly transmitted into the bloodstream.
Münch Jan   +10 more
doaj   +1 more source

The Platelet Receptor CLEC-2 Is Active as a Dimer

open access: yesBiochemistry, 2009
The platelet receptor CLEC-2 binds to the snake venom toxin rhodocytin and the tumor cell surface protein podoplanin. Binding of either of these ligands promotes phosphorylation of a single tyrosine residue in the YXXL motif in the intracellular domain of CLEC-2.
Watson, A.   +9 more
openaire   +3 more sources

Slot blot analysis of the effects of hematoporphyrin and 2CP on the binding of Fc-CLEC-2 to podoplanin.

open access: yes, 2019
(A) Slot blot analysis of the levels of podoplanin and CLEC-2 in the elution fraction from complexes formed in the presence or absence of the indicated concentrations of hematoporphyrin (HPy) or 2CP.
Yusuke Suzuki (525707)   +10 more
core   +1 more source

Lymphatic blood filling in CLEC-2-deficient mouse models

open access: yes, 2020
C-type lectin-like receptor 2 (CLEC-2) is considered as a potential drug target in settings of wound healing, inflammation, and infection. A potential barrier to this is evidence that CLEC-2 and its ligand podoplanin play a critical role in preventing ...
Babak J Mehrara (8530731)   +13 more
core   +1 more source

Elevated Soluble Podoplanin Associates with Hypercoagulability in Patients with Nephrotic Syndrome

open access: yesClinical and Applied Thrombosis/Hemostasis, 2022
Podoplanin (PDPN) promotes platelet aggregation and activation by interacting with C-type lectin-like receptor 2(CLEC-2) on platelets. The interaction between the upregulated PDPN and platelet CLEC-2 stimulates venous thrombosis. PDPN was identified as a
Ying Ji MD   +8 more
doaj   +1 more source

CLEC-2/PDPN signalling phospho proteomics

open access: yes, 2019
Fold difference values from TMT proteomics of total protein and phosphopeptides, 5 biological replicates: control vs CLEC-2 stimulated. 15 minutes and 24 hour time points.Relating to Figure 3dAbstractLymph nodes (LNs) work as filtering organs, constantly
Chris Tape (6782324)   +2 more
core   +1 more source

IgG Glycosylation‐Dependent CLEC7A Signaling Drives Podocyte Dysfunction in Lupus Nephritis

open access: yesArthritis &Rheumatology, EarlyView.
Objective Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE) that can lead to end‐stage kidney disease and increased mortality. IgG from patients with LN displays abnormal glycosylation, contributing to podocyte injury.
Rohit Upadhyay   +3 more
wiley   +1 more source

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