Ignet

Gene Information

Gene symbol: F2R

Gene name: coagulation factor II (thrombin) receptor

HGNC ID: 3537

Synonyms: TR, CF2R, PAR1, PAR-1

Related Genes

#	Gene Symbol	Number of hits
1	F2	1 hits
2	F2RL2	1 hits
3	F2RL3	1 hits
4	MARK2	1 hits
5	NPHS2	1 hits
6	PROCR	1 hits
7	VASP	1 hits

Related Sentences

#	PMID	Sentence
1	31339775	Given that T helper (CD4⁺) cells expressing IL-17A (so-called Th17 cells) have recently been reported to be resistant to GC treatment, and GC resistance remains a major challenge in the management of NS, we hypothesized that Th17 cells produce a circulating factor that is capable of signaling to the podocyte and inducing deleterious phenotypic changes.
2	31339775	This demonstrated that podocytes treated with Th17 cell culture supernatant, as well as with patient disease plasma, showed significant stimulation of JNK and p38 MAPK pathways and an increase in motility, which was blocked using a JNK inhibitor.
3	31339775	We have previously shown that nephrotic plasma elicits a podocyte response via protease-activated receptor-1 (PAR-1).
4	29110957	The kidney expresses protease-activated receptor-1 (PAR-1).
5	29110957	The kidney expresses protease-activated receptor-1 (PAR-1).
6	29110957	PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood.
7	29110957	PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood.
8	29110957	Pathological analysis showed that Q94 treatment significantly attenuated periodic acid-Schiff and desmin staining, indicators of podocyte injury, and also decreased glomerular levels of podocin and nephrin.
9	29110957	Pathological analysis showed that Q94 treatment significantly attenuated periodic acid-Schiff and desmin staining, indicators of podocyte injury, and also decreased glomerular levels of podocin and nephrin.
10	29110957	In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes.
11	29110957	In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes.
12	28424276	Using receptor-blocking antibodies and activation peptides, we determined that thrombin-mediated injury depended upon interactions between protease-activated receptor 3 and protease-activated receptor 4 in human podocytes, and between protease-activated receptor 1 and protease-activated receptor 4 in rat podocytes.
13	28424276	Using receptor-blocking antibodies and activation peptides, we determined that thrombin-mediated injury depended upon interactions between protease-activated receptor 3 and protease-activated receptor 4 in human podocytes, and between protease-activated receptor 1 and protease-activated receptor 4 in rat podocytes.
14	28424276	Proximity ligation and coimmunoprecipitation assays confirmed thrombin-dependent interactions between human protease-activated receptor 3 and protease-activated receptor 4, and between rat protease-activated receptor 1 and protease-activated receptor 4 in cultured podocytes.
15	28424276	Proximity ligation and coimmunoprecipitation assays confirmed thrombin-dependent interactions between human protease-activated receptor 3 and protease-activated receptor 4, and between rat protease-activated receptor 1 and protease-activated receptor 4 in cultured podocytes.
16	23436459	Active proteases in nephrotic plasma lead to a podocin-dependent phosphorylation of VASP in podocytes via protease activated receptor-1.
17	23436459	Active proteases in nephrotic plasma lead to a podocin-dependent phosphorylation of VASP in podocytes via protease activated receptor-1.
18	23436459	By the use of siRNA technology, we show that proteases in the plasma signal predominantly via protease activated receptor-1 (PAR1) to VASP.
19	23436459	By the use of siRNA technology, we show that proteases in the plasma signal predominantly via protease activated receptor-1 (PAR1) to VASP.
20	22117049	Thus, within the renal glomeruli, aPC preserves endothelial cells via a protease-activated receptor-1 (PAR-1) and endothelial protein C receptor-dependent mechanism.
21	22117049	While exploring the latter, we identified a novel aPC/PAR-dependent cytoprotective signaling mechanism.
22	22117049	In podocytes, aPC inhibits apoptosis through proteolytic activation of PAR-3 independent of endothelial protein C receptor.
23	22117049	PAR-3 is not signaling competent itself as it requires aPC-induced heterodimerization with PAR-2 (human podocytes) or PAR-1 (mouse podocytes).
24	22117049	Genetic deletion of PAR-3 impairs the nephroprotective effect of aPC, demonstrating the crucial role of PAR-3 for aPC-dependent podocyte protection.