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The protein encoded by SCARB2 is a type III glycoprotein that is located primarily in limiting membranes of lysosomes and endosomes. Additionally we are shipping SCARB2 Proteins (14) and SCARB2 Kits (7) and many more products for this protein.
Showing 10 out of 69 products:
Chinese Hamster Polyclonal SCARB2 Primary Antibody for ICC, FACS - ABIN152881
Huby, Doucet, Dachet, Ouzilleau, Ueda, Afzal, Rubin, Chapman, Lesnik: Knockdown expression and hepatic deficiency reveal an atheroprotective role for SR-BI in liver and peripheral tissues. in The Journal of clinical investigation 2006
Show all 12 Pubmed References
Dog (Canine) Polyclonal SCARB2 Primary Antibody for ICC, IF - ABIN152898
Balreira, Gaspar, Caiola, Chaves, Beirão, Lima, Azevedo, Miranda: A nonsense mutation in the LIMP-2 gene associated with progressive myoclonic epilepsy and nephrotic syndrome. in Human molecular genetics 2008
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Human Polyclonal SCARB2 Primary Antibody for ELISA, WB - ABIN1002736
Fujita, Ezaki, Noguchi, Kono, Himeno, Kato: Isolation and sequencing of a cDNA clone encoding 85kDa sialoglycoprotein in rat liver lysosomal membranes. in Biochemical and biophysical research communications 1991
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Mouse (Murine) Polyclonal SCARB2 Primary Antibody for CyTOF, FACS - ABIN5500392
Yamayoshi, Koike: Identification of a human SCARB2 region that is important for enterovirus 71 binding and infection. in Journal of virology 2011
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Human Polyclonal SCARB2 Primary Antibody for IHC (p), IHC - ABIN449974
Berkovic, Dibbens, Oshlack, Silver, Katerelos, Vears, Lüllmann-Rauch, Blanz, Zhang, Stankovich, Kalnins, Dowling, Andermann, Andermann, Faldini, DHooge, Vadlamudi, Macdonell, Hodgson, Bayly, Savige et al.: Array-based gene discovery with three unrelated subjects shows SCARB2/LIMP-2 deficiency causes myoclonus epilepsy and glomerulosclerosis. ... in American journal of human genetics 2008
Human Polyclonal SCARB2 Primary Antibody for IHC, ELISA - ABIN361195
Murphy, Gysbers, Abbott, Tayebi, Kim, Sidransky, Cooper, Garner, Halliday: Reduced glucocerebrosidase is associated with increased ?-synuclein in sporadic Parkinson's disease. in Brain : a journal of neurology 2014
This work describes a novel function for the Scarb2 receptor as an essential glycoprotein for notochord development.
The binding of a monoclonal antibody to the apical region of SCARB2 blocks EV71 infection.
The findings identify SR-BII as a functional SAA (show SAA1 Antibodies) receptor that mediates SAA (show SAA1 Antibodies) uptake and contributes to its proinflammatory signaling via the MAPK (show MAPK1 Antibodies)-mediated signaling pathways.
In this paper we provide an updated overview of the clinical and genetic features of SCARB2-related PME (show CSTB Antibodies) and on the functions of the LIMP2 protein [review]
neutrophils are able to drive a macrophage activation that would regulate the increase in LIMP-2 expression during the early phase of Cer (show CBLN1 Antibodies)-induced acute pancreatitis
Findings suggested that STX1B (show STX1B Antibodies) rs4889603, FAM47E rs6812193 and SCARB2 rs6825004 do not confer a significant risk for Parkinson's disease
LIMPII was increased greater than twofold in urinary microvesicles obtained from patients with idiopathic membranous nephropathy compared to microvesicles of patients with idiopathic focal segmental glomerulosclerosis and normal controls.
hSR-BII (show CACNA1E Antibodies), and to a lesser extent hSR-BI, significantly increase LPS (show IRF6 Antibodies)-induced inflammation and contribute to LPS (show IRF6 Antibodies)-induced tissue injury in the liver and kidney, two major organs susceptible to LPS (show IRF6 Antibodies) toxicity.
Although hrGCase cellular uptake is independent of LIMP-2, its trafficking to the lysosomes is mediated by this receptor.
SNCA and SCARB2 loci are also associated with dementia with Lewy bodies, after a study-wise Bonferroni correction, although these have a different association profile than the associations reported for the same loci in Parkinson's.
a novel mutation in SCARB2 as a cause of progressive myoclonus epilepsy in China
AP-3 (show AP3B1 Antibodies)-dependent LB targeting is facilitated by protein/protein interaction between LIMP-2/SCARB2 and PRDX6 (show PRDX6 Antibodies) in vitro and in vivo
Heterologous expression of the luminal domain of LIMP-2 in wild-type cells.
In LIMP-2-deficient brains a significant reduction in GC activity led to lipid storage, disturbed autophagic/lysosomal function, and alpha-synuclein accumulation.
absence of Limp-2 reduces inflammation in experimental crescentic glomerulonephritis with decreased macrophage and T-cell infiltration in the kidney.
Limp-2 deficiency leads to a minor increase in circulating renin (show REN Antibodies). Limp-2, however, is not required for acute or chronic stimulation of renin (show REN Antibodies) release.
The SR-BII is involved in cholesterol ester uptake for steroidogenesis and spermatogenesis in the testis.
The residues between 144 and 151 are critical for SCARB2 binding to VP1 of EV71 and seven residues from the human receptor could convert murine SCARB2, an otherwise inefficient receptor, to an efficient receptor for EV71 viral infection.
The data suggest that tubular proteinuria in Limp-2(-/-) mice is due to failure of endosomes containing reabsorbed proteins to fuse with lysosomes in the proximal tubule of the kidney. Failure of proteolysis is a novel mechanism for tubular proteinuria.
The coiled-coil structure of LIMP-2 is required for its interaction with beta-glucocerebrosidase (show GBA Antibodies).
The protein encoded by this gene is a type III glycoprotein that is located primarily in limiting membranes of lysosomes and endosomes. Earlier studies in mice and rat suggested that this protein may participate in membrane transportation and the reorganization of endosomal/lysosomal compartment. The protein deficiency in mice was reported to impair cell membrane transport processes and cause pelvic junction obstruction, deafness, and peripheral neuropathy. Further studies in human showed that this protein is a ubiquitously expressed protein and that it is involved in the pathogenesis of HFMD (hand, foot, and mouth disease) caused by enterovirus-71 and possibly by coxsackievirus A16. Mutations in this gene caused an autosomal recessive progressive myoclonic epilepsy-4 (EPM4), also known as action myoclonus-renal failure syndrome (AMRF). Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
CD36 antigen (collagen type I receptor, thrombospondin receptor)-like 2
, CD36 antigen-like 2
, lysosome membrane protein 2
, scavenger receptor class B, member 2
, lysosome membrane protein 2-like
, putative lysosomal integral membrane protein II
, 85 kDa lysosomal membrane sialoglycoprotein
, 85 kDa lysosomal sialoglycoprotein scavenger receptor class B, member 2
, CD36 antigen (collagen type I receptor, thrombospondin receptor)-like 2 (lysosomal integral membrane protein II)
, LIMP II
, lysosome membrane protein II