anti-Fibrinogen-Like 2 (FGL2) Antibodies

Human Fibrinogen-Like 2 (FGL2) interaction partners

1. The increase in intrahepatic and plasma sFGL2 by Tregs may restrict AIH progression by inhibiting conventional CD8+ T cells and Tc17 cell function. The high correlation between sFGL2 and disease severity may predict AIH outcome.

2. The presence of infectious/autoimmune diseases does not significantly alter FGL2 activity in the peripheral blood

3. FGL2 expression is a novel, independent, and an adverse prognostic factor of clinical outcomes in patients with clear cell renal cell carcinoma.

4. Serum FGL2 is a promising biomarker for assessing the severity and prognosis in severe TBI

5. FGL2 promotes tumor progression in the brain by suppressing CD103-expressing dendritic cell differentiation.

6. serum levels of soluble FAS ligand (sFASL) and interferon gamma (IFN-gamma) were analyzed and correlated with sFGL2 levels in Hepatitis C Virus-Infected Patients and Hepatocellular Carcinoma Patients.

7. Data suggest that fibrinogen-like protein 2 (hFGL2) gene silencing via miRNA may be an alternative strategy for the management of hepatocellular carcinoma (HCC).

8. Our results identified FGL2, GAL, SEMA4D, SEMA7A, and IDO1 as new candidate genes that could be involved in MSCs-mediated immunomodulation. FGL2, GAL, SEMA4D, SEMA7A, and IDO1 genes appeared to be differentially transcribed in the different MSC populations. Moreover, these genes were not similarly modulated following MSCs-exposure to inflammatory signals

9. Report increased expression of FGL-2 in peripheral blood mononuclear cells from mycosis fungoides patients.

10. these results suggest that FGL-2 mediates angiogenesis and tumorigenesis not by thrombin-mediated mechanism but rather through FGF-2/ERK signaling pathway.

11. Results show that FGL2 functions as a key immune-suppressive modulator and has potential as an immunotherapeutic target for treating glioblastoma multiforme (GBM).

12. FGL-2 prothrombinase activity in PBMC of lymphoma patients is increased in active disease and normalizes during remission, thus being a potential marker for follow up of lymphoma patients.

13. Studied fibrinogen-like protein 2 expression and its role in CRC metastasis and underlying molecular mechanisms; results suggest that FGL2 plays an important oncogenic role in CRC aggressiveness by inducing EMT.

14. The selected peptide sequence NPG-12 may be a critical domain for hfgl2 prothrombinase activity.

15. The proliferation index of CD8(+)T cells after blocking FGL2 was higher.

16. immunomodulatory activity of FGL2 may be involved in the immunopathogenesis of inflammatory bowel disease

17. Circulating fibrinogen-like protein 2 is increased in patients with systemic sclerosis.

18. Serum fgl2 levels were increased among renal allograft recipients with acute rejection episodes to an extent dependent upon the pathological type and severity of the response.

19. FGL2 contributes to hepatocellular carcinoma tumour growth and angiogenesis in a thrombin-dependent manner, and downregulation of its expression might be of therapeutic significance in HCC.

20. HBV surface antigen-induced transcription of hfgl2 prothrombinase gene.

Pig (Porcine) Fibrinogen-Like 2 (FGL2) interaction partners

1. soluble FGL2 might be a potential renoprotective mediator involved in the renal self-repairing and remodeling.

2. studies of pig-to-baboon kidney xenografts undergoing acute vascular rejection in vivo revealed induction of pfgl2 expression on graft vascular endothelial cells.

Mouse (Murine) Fibrinogen-Like 2 (FGL2) interaction partners

1. In the mouse fulminant hepatitis (FH) model revealed that CC10 protects against MHV-3-induced FH via suppression of Fgl2 expression in macrophages. In vitro, CC10 was found to significantly inhibit the expression of Fgl2 in MHV-3-infected mouse peritoneal macrophages. Such effects may be mediated by the transcription factor HBP1.

2. The increase in intrahepatic and plasma sFGL2 by Tregs may restrict AIH progression by inhibiting conventional CD8+ T cells and Tc17 cell function. The high correlation between sFGL2 and disease severity may predict AIH outcome.

3. our results presented herein point to Fgl2 as a novel protective molecule in the pathogenesis of IBD. We found that Fgl2 is critical for limiting DSS-induced colitis and subsequent CAC development through its effects on macrophage polarization

4. These results indicated that FGL2 might be a promising target for attenuating the severity of Severe acute pancreatitis (SAP) and adenovirus-mediated artificial miRNAs targetting FGL2 represented a potential therapeutic approach for the treatment of SAP.

5. The results of the present study indicated that, in the colitis model, FGL2 was associated with the immunopathogenesis of inflammatory bowel disease.

6. FGL2-overexpressing regulatory T-cells have enhanced immunosuppressive activity and prevent colitis; FGL2-over-expressing effector T-cells are hypo-proliferative and do not induce colitis

7. PD-1 plays a vital role in brain inflammation via regulation of Fgl-2 after ICH, and that manipulation of PD-1 might be a promising therapeutical target in ICH.

8. In vitro IL-33 treatment abrogated MHV-3 and IFN-gamma induced FGL2 expression in RAW264.7 and THP-1 cells.

9. FGL2 appears as one of the key players in immune regulatory processes favoring metacestode survival by promoting Regulatory T-cell activity and IL-17A production that contributes to FGL2-regulation.

10. TNF-alpha, and FGL2 form an integral network that contributes to coagulation and complement activation, and suggest that those are potential therapeutic targets in viral FH intervention.

11. these data strongly suggest that Treg cells expressing FGL2 mediate rapamycin-induced tolerance. Furthermore, a gene biomarker panel that includes fgl2 can distinguish between rejecting and tolerant grafts.

12. Combined adenovirus-mediated artificial microRNAs targeting mfgl2, mFas, and mTNFR1 protect against fulminant hepatic failure in mice.

13. Mouse susceptibility to MHV-3-induced fulminant hepatitis may rely on C5a/C5aR interactions, for which ERK1/2 and p38 pathways participate in up-regulating Fgl2 expression.

14. Targeted deletion of FGL2 leads to increased early viral replication and enhanced adaptive immunity in a murine model of acute viral hepatitis.

15. Cysteines at positions 94, 97, 184 and 187, found in the coiled-coil domain were shown to be crucial for FGL2 oligomerization.

16. FGL2 binding to the FcgammaRIIB receptor expressed on sinusoidal endothelial cells (SECs) is a critical event in the initiation of the hepatic reperfusion injury cascade through induction of SEC and hepatocyte death.

17. The prothrombinase activity of FGL2 contributes to the pathogenesis of experimental arthritis.

18. Fgl2 cleaves prothrombin to thrombin consistent with serine protease activity and requires calcium, phospholipids, and factor Va for its full activity.

19. While membrane-bound Fgl2 acts as a prothrombinase, soluble Fgl2 is an immunomodulatory protein that has the ability to modulate T cell responses and to alter dendritic cell (DC) maturation to favor production of tolerogenic DC.

20. fgl2 expression in endothelial cells is controlled by Ets-1 and Oct-1, and requires Sp1 and Sp3