Ignet

Gene Information

Gene symbol: LAMB2

Gene name: laminin, beta 2 (laminin S)

HGNC ID: 6487

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	ACTN4	1 hits
3	CD2AP	1 hits
4	COL1A1	1 hits
5	COL4A3	1 hits
6	COL4A4	1 hits
7	COL4A5	1 hits
8	IGF2	1 hits
9	IGF2BP2	1 hits
10	LAMB1	1 hits
11	LMX1B	1 hits
12	NPHS1	1 hits
13	NPHS2	1 hits
14	PLCL1	1 hits
15	TRPC6	1 hits
16	UMOD	1 hits
17	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
2	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
3	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
4	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
5	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
6	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
7	16752799	Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2.
8	16752799	Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes.
9	16752799	It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2).
10	16752799	This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele.
11	16752799	There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models).
12	17267748	Aside from the delay in podocyte maturation, DDS glomeruli show swollen endothelial cells, reminiscent of endotheliosis, together with incompletely fused capillary basement membranes; a dramatic decrease in collagen alpha4(IV) and laminin beta2 chains; and the presence of immature or activated mesangial cells that express alpha-smooth muscle actin.
13	19562370	Here, we describe already well-characterized genetic diseases due to mutations in nephrin, podocin, CD2AP, alpha-actinin-4, WT1, and laminin beta2 chain, as well as more recently identified genetic abnormalities in TRPC6, phospholipase C epsilon, and the proteins encoded by the mitochondrial genome.
14	21327778	Of these nine proteins, mutations in the genes encoding four of them (LAMB2, COL4A3, COL4A4, and COL4A5) cause glomerular disease in humans as well as in mice.
15	21876163	Forced expression of laminin beta1 in podocytes prevents nephrotic syndrome in mice lacking laminin beta2, a model for Pierson syndrome.
16	21876163	These results suggest the possibility that up-regulation of LAMB1 in podocytes, should it become achievable, would likely lessen the severity of nephrotic syndrome in patients carrying LAMB2 mutations.
17	21876163	Forced expression of laminin beta1 in podocytes prevents nephrotic syndrome in mice lacking laminin beta2, a model for Pierson syndrome.
18	21876163	These results suggest the possibility that up-regulation of LAMB1 in podocytes, should it become achievable, would likely lessen the severity of nephrotic syndrome in patients carrying LAMB2 mutations.
19	22683419	The GBM is assembled through an interweaving of type IV collagen with laminins, nidogen, and sulfated proteoglycans.
20	22683419	Mutations in genes encoding LAMB2, COL4A3, COL4A4, and COL4A5 cause glomerular disease in humans as well as in mice.
21	24461191	Among the identified genes mutated in podocytes include NPHS2, NPHS1, WT1, TRPC6, MDR1, PLCE1, LMX1B, and LAMB2.
22	27442391	Hildebrandt's group has shown that 85% of the SRNS cases with onset by 3 months of age and 66% with onset by 1 year of age can be explained by recessive mutations in one of four genes only (NPHS1, NPHS2, LAMB2, or WT1).
23	27442391	This is very important for patients who carry mutations in a gene of coenzyme Q10 biosynthesis (COQ2, COQ6, ADCK4, or PDSS2).
24	30099615	Mutations in nephrin (NPHS1), podocin (NPHS2), laminin β2 (LAMB2), and α-actinin-4 (ACTN4) have been shown to induce ER stress in HEK293 cells and podocytes in hereditary nephrotic syndromes; various founder mutations in collagen IV α chains (COL4A) have been demonstrated to activate podocyte ER stress in collagen IV nephropathies; and mutations in uromodulin (UMOD) have been reported to trigger tubular ER stress in autosomal dominant tubulointerstitial kidney disease.
25	30099615	Recently, we have identified mesencephalic astrocyte-derived neurotrophic factor (MANF) and cysteine-rich with EGF-like domains 2 (CRELD2) as urinary ER stress biomarkers in ER stress-mediated kidney diseases.
26	32437062	Long noncoding RNA Airn protects podocytes from diabetic nephropathy lesions via binding to Igf2bp2 and facilitating translation of Igf2 and Lamb2.
27	32437062	Mechanistically, using RNA immunoprecipitation and RNA pull-down assays, we found that Airn could bind to the RNA-binding protein Igf2bp2, thus facilitating translation of Igf2 and Lamb2 to maintain normal podocyte viability and glomerular barrier function.
28	32437062	Long noncoding RNA Airn protects podocytes from diabetic nephropathy lesions via binding to Igf2bp2 and facilitating translation of Igf2 and Lamb2.
29	32437062	Mechanistically, using RNA immunoprecipitation and RNA pull-down assays, we found that Airn could bind to the RNA-binding protein Igf2bp2, thus facilitating translation of Igf2 and Lamb2 to maintain normal podocyte viability and glomerular barrier function.