Browse our anti-Gardner-Rasheed Feline Sarcoma Viral (V-Fgr) Oncogene Homolog (FGR) Antibodies

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 (show PTAFR Antibodies) and FGR as the most important hub genes for predicting patient survival.

2. the Src (show SRC Antibodies) tyrosine kinase (show TXK Antibodies) 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 (show HCK Antibodies) and FGR in FCRL4 (show FCRL4 Antibodies)-mediated immunoregulation and for the functional importance of posttranslational modifications of the FCRL4 (show FCRL4 Antibodies) molecule.

4. Data indicate that combined treatment using SFK (LYN (show LYN Antibodies), HCK (show HCK Antibodies), or FGR) and c-KIT (show KIT Antibodies) inhibitor dasatinib dasatinib and chemotherapy provides a novel approach to increasing p53 (show TP53 Antibodies) activity and enhancing targeting of acute myeloid leukemia (show BCL11A Antibodies) (AML (show RUNX1 Antibodies)) stem cells.

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

6. Recruitment of the coactivator, SRC2 (show NCOA2 Antibodies), is coupled to cooperative DNA binding by the progesterone receptor (show PGR Antibodies).

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

1. the Hck (show HCK Antibodies), Fgr and Lyn (show LYN Antibodies) kinases are also necessary for amastigote uptake by macrophages. Src (show SRC Antibodies)-mediated Arg activation is required for efficient uptake.

2. Data indicate that Src (show SRC Antibodies)-Family Kinases Hck (show HCK Antibodies) 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 (show SRC Antibodies) family kinases Hck (show HCK Antibodies), Fgr, and Lyn (show LYN Antibodies) 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 (show HCK Antibodies)/Lyn (show LYN Antibodies)-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 (show CLNK Antibodies) with Fgr, mediated by the C-terminal proline-rich region of MIST (show CLNK Antibodies) and the SH3 domain (show ITSN1 Antibodies) of Fgr, was required for the suppression of NK-cell receptor (show KLRD1 Antibodies)-induced IFN-gamma (show IFNG Antibodies) 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.