Ignet

Gene Information

Gene symbol: FCGR3A

Gene name: Fc fragment of IgG, low affinity IIIa, receptor (CD16a)

HGNC ID: 3619

Synonyms: CD16, CD16a

Related Genes

#	Gene Symbol	Number of hits
1	ABL1	1 hits
2	CD68	1 hits
3	CDKN1A	1 hits
4	CSF3	1 hits
5	INPPL1	1 hits
6	NCAM1	1 hits
7	NPHS1	1 hits
8	PODXL	1 hits
9	RAPH1	1 hits
10	SLC4A1	1 hits
11	SLC4A3	1 hits
12	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
2	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
3	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
4	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
5	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
6	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
7	29416010	However, the relationship between nephrin and c-Abl was unknown.
8	29416010	However, the relationship between nephrin and c-Abl was unknown.
9	29416010	However, the relationship between nephrin and c-Abl was unknown.
10	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
11	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
12	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
13	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
14	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
15	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
16	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
17	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
18	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
19	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
20	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
21	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
22	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
23	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
24	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
25	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
26	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
27	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
28	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
29	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
30	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
31	28408238	Novel roles for podocalyxin in regulating stress myelopoiesis, Rap1a, and neutrophil migration.
32	28408238	At steady state, Podxl expression among hematopoietic progenitor cells was low level but was induced by granulocyte colony-stimulating factor (G-CSF) in myeloid progenitors and by thrombopoietin in human stem cells.
33	28408238	Within bone marrow (and after G-CSF challenge), Podxl deletion moderately decreased colony forming units-granulocytes, eyrthrocytes, monocyte/macrophages, megakaryocytes and CD16/32^posCD11b^pos progenitors but did not affect Gr-1^pos cell populations.
34	28408238	In bone marrow human progenitor cells, Podxl-KO led to heightened G-CSF activation of Rap1a^GTP, and Rap1a^GTP inhibition attenuated Podxl-KO neutrophil migration.
35	28318628	There was a significantly decreased percentage of natural killer (NK) cells with an increase in the CD56^brightCD16^-/lo NK subset.
36	28318628	There was a significantly decreased percentage of natural killer (NK) cells with an increase in the CD56^brightCD16^-/lo NK subset.
37	28318628	There were a significantly decreased percentage of regulatory T cells, together with an increased plasma concentration of TNF-alpha, IL-5 and IL-2RA.
38	28318628	There were a significantly decreased percentage of regulatory T cells, together with an increased plasma concentration of TNF-alpha, IL-5 and IL-2RA.
39	28318628	After rituximab, B-cell recovery was still incomplete at six months, with persistent alterations of B-cell subsets, a significant increase of both T-regulatory (Treg) cells and NK cells, and a significant decrease of both the CD56^brightCD16^-/lo NK subset and TNF-alpha levels.
40	28318628	After rituximab, B-cell recovery was still incomplete at six months, with persistent alterations of B-cell subsets, a significant increase of both T-regulatory (Treg) cells and NK cells, and a significant decrease of both the CD56^brightCD16^-/lo NK subset and TNF-alpha levels.
41	22194892	Nephrin regulates lamellipodia formation by assembling a protein complex that includes Ship2, filamin and lamellipodin.
42	22194892	Nephrin regulates lamellipodia formation by assembling a protein complex that includes Ship2, filamin and lamellipodin.
43	22194892	Upon activation Nephrin recruits and regulates a protein complex that includes Ship2 (SH2 domain containing 5' inositol phosphatase), Filamin and Lamellipodin, proteins important in regulation of actin and focal adhesion dynamics, as well as lamellipodia formation.
44	22194892	Upon activation Nephrin recruits and regulates a protein complex that includes Ship2 (SH2 domain containing 5' inositol phosphatase), Filamin and Lamellipodin, proteins important in regulation of actin and focal adhesion dynamics, as well as lamellipodia formation.
45	22194892	Using the previously described CD16-Nephrin clustering system, Nephrin ligation or activation resulted in phosphorylation of the actin crosslinking protein Filamin in a p21 activated kinase dependent manner.
46	22194892	Using the previously described CD16-Nephrin clustering system, Nephrin ligation or activation resulted in phosphorylation of the actin crosslinking protein Filamin in a p21 activated kinase dependent manner.
47	22194892	In the CD16-Nephrin clustering model, Nephrin ligation resulted in abnormal morphology of actin tails in human podocytes when Ship2, Filamin or Lamellipodin were individually knocked down.
48	22194892	In the CD16-Nephrin clustering model, Nephrin ligation resulted in abnormal morphology of actin tails in human podocytes when Ship2, Filamin or Lamellipodin were individually knocked down.
49	11158216	Immunohistochemistry and confocal laser microscopy carried out on kidneys with FSGS relapse disclosed several phenomena. (1) Some podocytes that expressed podocalyxin, synaptopodin, and glomerular epithelial protein-1 were detached from the tuft and were free in the urinary space. (2) In the cellular variant, most podocytes had lost podocyte-specific epitopes (podocalyxin, synaptopodin, glomerular epithelial protein-1, Wilm's tumor protein-1, complement receptor-1, and vimentin).
50	11158216	In the scar variant, these podocyte markers were absent from cobblestone-like epithelial cells and from pseudotubules. (3) Podocytes had acquired expression of various cytokeratins (CK; identified by the AE1/AE3, C2562, CK22, and AEL-KS2 monoclonal antibodies) that were not found in the podocytes of control glomeruli.
51	11158216	Parietal epithelial cells expressed AE1/AE3 CK that were faintly, if ever, found on the parietal epithelial cells of normal glomeruli. (4) Numerous cells located at the periphery of the tuft or free in Bowman's space and within tubular lumens expressed macrophagic epitopes (identified by PGM1 [CD68], HAM56, and 25F9 monoclonal antibodies).
52	11158216	These macrophage-like cells expressed the activation epitopes HLA-DR and CD16. (5) A number of these cells coexpressed podocalyxin + AE1/AE3 CK, podocalyxin + CD68, and CD68 + AE1/AE3.