Ignet

Gene Information

Gene symbol: ACTN4

Gene name: actinin, alpha 4

HGNC ID: 166

Related Genes

#	Gene Symbol	Number of hits
1	ACTB	1 hits
2	APOL1	1 hits
3	CAPG	1 hits
4	CCL2	1 hits
5	CCL5	1 hits
6	CFH	1 hits
7	CX3CL1	1 hits
8	ICAM1	1 hits
9	IL18	1 hits
10	IL1B	1 hits
11	IL6	1 hits
12	KIRREL	1 hits
13	LASP1	1 hits
14	LMX1B	1 hits
15	MCKD1	1 hits
16	MSN	1 hits
17	MYH14	1 hits
18	MYH7	1 hits
19	NPHS1	1 hits
20	PTPRO	1 hits
21	RPS27A	1 hits
22	SMAD7	1 hits
23	SYNPO	1 hits
24	TGFB1	1 hits
25	TJP1	1 hits
26	TMOD3	1 hits
27	TNF	1 hits
28	TRPC6	1 hits
29	TUBB2A	1 hits
30	TUBB3	1 hits
31	TUBB4	1 hits
32	VCL	1 hits

Related Sentences

#	PMID	Sentence
1	2265390	Recurrence of disease is a common histologic finding in many transplant recipients but, except for a few diseases such as HUS, FSGS, and oxalosis, it usually does not lead to graft failure.
2	12397035	Smad6 and Smad7 are inhibitory SMADs with putative functional roles at the intersection of major intracellular signaling networks, including TGF-beta, receptor tyrosine kinase (RTK), JAK/STAT, and NF-kappaB pathways.
3	12397035	This study reports differential functional roles and regulation of Smad6 and Smad7 in TGF-beta signaling in renal cells, in murine models of renal disease and in human glomerular diseases.
4	12397035	Smad7 is upregulated in podocytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and diabetic nephropathy [DN]) with a statistically significant upregulation in "classical" podocyte-diseases such as FSGS and MCD.
5	12397035	TGF-beta induces Smad7 synthesis in cultured podocytes and Smad6 synthesis in cultured mesangial cells.
6	12397035	Although Smad7 expression inhibited both Smad2- and Smad3-mediated TGF-beta signaling in podocytes, it inhibited only Smad3 but not Smad2 signaling in mesangial cells.
7	12397035	In contrast, Smad6 had no effect on TGF-beta/Smad signaling in podocytes and enhanced Smad3 signaling in mesangial cells.
8	12397035	These data suggest that Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity, whereas Smad6 has no role in TGF-beta response and injury in podocytes.
9	12397035	These data indicate an important role for Smad6 and Smad7 in glomerular cells in vivo that could be important for the cell homeostasis in physiologic and pathologic conditions.
10	15208719	We used cells from these mice to show increased degradation of mutant alpha-actinin-4, mediated, at least in part, by the ubiquitin-proteasome pathway.
11	18838678	Combination therapy with AT1 blocker and vitamin D analog markedly ameliorates diabetic nephropathy: blockade of compensatory renin increase.
12	18838678	Here we demonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabetes model due to the blockade of the compensatory renin rise by the vitamin D analog, leading to more effective RAS inhibition.
13	18838678	STZ-treated diabetic DBA/2J mice developed progressive albuminuria and glomerulosclerosis within 13 weeks, accompanied by increased intrarenal production of angiotensin (Ang) II, fibronection, TGF-beta, and MCP-1 and decreased expression of slit diaphragm proteins.
14	18838678	The combined treatment suppressed the induction of fibronection, TGF-beta, and MCP-1 and reversed the decline of slit diaphragm proteins nephrin, Neph-1, ZO-1, and alpha-actinin-4.
15	18838678	These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan.
16	21136853	In T1DM with DN, beta-actin and three isoforms of tubulin beta-2 chain, tropomodulin-3, and LASP-1 were decreased, whereas two tubulin beta-4 chain isoforms, one alpha actinin-4 isoform, membrane-organizing extension spike protein (MOESIN), FLJ00279 (corresponding to a fragment of myosin heavy chain, non-muscle type A), vinculin, a tropomyosin isoform, and the macrophage capping protein were increased.
17	21537349	This Review, therefore, focuses on key proinflammatory molecules and pathways implicated in the development and progression of diabetic nephropathy: the chemokines CCL2, CX3CL1 and CCL5 (also known as MCP-1, fractalkine and RANTES, respectively); the adhesion molecules intercellular adhesion molecule 1, vascular cell adhesion protein 1, endothelial cell-selective adhesion molecule, E-selectin and α-actinin 4; the transcription factor nuclear factor κB; and the inflammatory cytokines IL-1, IL-6, IL-18 and tumor necrosis factor.
18	21997392	Compared with normal glomeruli, fewer cells stained for APOL1 in FSGS and HIVAN glomeruli, even when expression of the podocyte markers GLEPP1 and synaptopodin appeared normal.
19	21997392	Unexpectedly, in both FSGS and HIVAN but not normal kidneys, the media of medium artery and arterioles contained a subset of α-smooth muscle actin-positive cells that stained for APOL1.
20	21997394	In summary, African Americans carrying two APOL1 risk alleles have a greatly increased risk for glomerular disease, and APOL1-associated FSGS occurs earlier and progresses to ESRD more rapidly.
21	23689571	Screening of ACTN4 and TRPC6 mutations in a Chinese cohort of patients with adult-onset familial focal segmental glomerulosclerosis.
22	23868926	An expanding universe of FSGS genes and phenotypes: LMX1B mutations cause familial autosomal dominant FSGS lacking extrarenal manifestations.