anti-Gardner-Rasheed Feline Sarcoma Viral (V-Fgr) Oncogene Homolog (FGR) 抗体产品概述

Human Gardner-Rasheed Feline Sarcoma Viral (V-Fgr) Oncogene Homolog (FGR) interaction partners

1. Weighted gene co-expression network analysis of gene modules for the prognosis of esophageal cancer yielded PTAFR and FGR as the most important hub genes for predicting patient survival.

2. the Src tyrosine kinase Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog (FGR) is associated with suberoylanilide hydroxamic acid resistance.

3. we provide evidence for involvement of HCK and FGR in FCRL4-mediated immunoregulation and for the functional importance of posttranslational modifications of the FCRL4 molecule.

4. Data indicate that combined treatment using SFK (LYN, HCK, or FGR) and c-KIT inhibitor dasatinib dasatinib and chemotherapy provides a novel approach to increasing p53 activity and enhancing targeting of acute myeloid leukemia (AML) stem cells.

5. Fgr plays a biologically significant role in ovarian cancer growth and might represent an important target

6. Substitution of two relevant serines with glutamic acid residues in urokinase prevents urokinase activation of p55fgr needed for cell migration and adhesion.

7. Recruitment of the coactivator, SRC2, is coupled to cooperative DNA binding by the progesterone receptor.

Mouse (Murine) Gardner-Rasheed Feline Sarcoma Viral (V-Fgr) Oncogene Homolog (FGR) interaction partners

1. the Hck, Fgr and Lyn kinases are also necessary for amastigote uptake by macrophages. Src-mediated Arg activation is required for efficient uptake.

2. Data indicate that Src-Family Kinases Hck and Fgr regulate cytokine secretion by macrophages.

3. Fgr is not only are progressively overexpressed in atherosclerosis, but it also controls critical molecular processes in monocyte influx, blood monocyte subset balance, macrophage accumulation, and the maintenance of atherosclerotic lesion stability.

4. Ablation of Fgr abolishes the capacity of mitochondria to adjust metabolism upon nutrient restriction, hypoxia/reoxygenation, and T cell activation, demonstrating the physiological relevance of this adaptive response.

5. The Src family kinases Hck, Fgr, and Lyn are critical for the generation of the in vivo inflammatory environment without a direct role in leukocyte recruitment.

6. The Src family kinase Fgr is critical for activation of mast cells and IgE-mediated anaphylaxis in mice.

7. Despite possessing enhanced killing, alveolar macrophage Fgr/Hck/Lyn-deficient ("triple-knockout") mice do not demonstrate enhanced inflammatory responses to Pneumocystis murina.

8. Hck and Fgr function as negative regulators of myeloid cell chemokine signaling by maintaining the tonic phosphorylation of PIR-

9. interaction of MIST with Fgr, mediated by the C-terminal proline-rich region of MIST and the SH3 domain of Fgr, was required for the suppression of NK-cell receptor-induced IFN-gamma production

10. Fgr plays no role in chemoattractant-induced, inside-out beta 2 integrin activation of neutrophils but regulates their outside-in, signaling-dependent sustained adhesion.

11. Data show that a pathway involving Fgr, DAP12 and FcRgamma is involved in the initial signaling events downstream of E-selectin-engaged PSGL-1 that are required to initiate neutrophil slow rolling.