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

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

4. Data indicate that combined treatment using SFK (LYN (显示 LYN 抗体), HCK (显示 HCK 抗体), or FGR) and c-KIT (显示 KIT 抗体) inhibitor dasatinib dasatinib and chemotherapy provides a novel approach to increasing p53 (显示 TP53 抗体) activity and enhancing targeting of acute myeloid leukemia (显示 BCL11A 抗体) (AML (显示 RUNX1 抗体)) 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 (显示 NCOA2 抗体), is coupled to cooperative DNA binding by the progesterone receptor (显示 PGR 抗体).

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

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

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