Search results for: APOL1 Antibody
#34316015 2021/07/27 To Up
Structures of the ApoL1 and ApoL2 N-terminal domains reveal a non-classical four-helix bundle motif.Apolipoprotein L1 (ApoL1) is a circulating innate immunity protein protecting against trypanosome infection. However, two ApoL1 coding variants are associated with a highly increased risk of chronic kidney disease. Here we present X-ray and NMR structures of the N-terminal domain (NTD) of ApoL1 and of its closest relative ApoL2. In both proteins, four of the five NTD helices form a four-helix core structure which is different from the classical four-helix bundle and from the pore-forming domain of colicin A. The reactivity with a conformation-specific antibody and structural models predict that this four-helix motif is also present in the NTDs of ApoL3 and ApoL4, suggesting related functions within the small ApoL family. The long helix 5 of ApoL1 is conformationally flexible and contains the BH3-like region. This BH3-like Î±-helixÂ resembles true BH3 domains only in sequence and structure but not in function, since it does not bind to the pro-survival members of the Bcl-2 family, suggesting a Bcl-2-independent role in cytotoxicity. These findings should expedite a more comprehensive structural and functional understanding of the ApoL immune protein family.
Mark Ultsch, Michael J Holliday, Stefan Gerhardy, Paul Moran, Suzie J Scales, Nidhi Gupta, Francesca Oltrabella, Cecilia Chiu, Wayne Fairbrother, Charles Eigenbrot, Daniel Kirchhofer
2510 related Products with: Structures of the ApoL1 and ApoL2 N-terminal domains reveal a non-classical four-helix bundle motif.100μg100 ug0.1ml (2mg/ml)100ug25 mg100ug100μl100 μg100ug100 ug100ul
#34138902 2021/06/17 To Up
Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.The mechanism of pathogenesis associated with APOL1 polymorphisms and risk for non-diabetic chronic kidney disease (CKD) is not fully understood. Prior studies have minimized a causal role for the circulating APOL1 protein, thus efforts to understand kidney pathogenesis have focused on APOL1 expressed in renal cells. Of the kidney cells reported to express APOL1, the proximal tubule expression patterns are inconsistent in published reports, and whether APOL1 is synthesized by the proximal tubule or possibly APOL1 protein in the blood is filtered and reabsorbed by the proximal tubule remains unclear. Using both protein and mRNA in situ methods, the kidney expression pattern of APOL1 was examined in normal human and APOL1 bacterial artificial chromosome transgenic mice with and without proteinuria. APOL1 protein and mRNA was detected in podocytes and endothelial cells, but not in tubular epithelia. In the setting of proteinuria, plasma APOL1 protein did not appear to be filtered or reabsorbed by the proximal tubule. A side-by-side examination of commercial antibodies used in prior studies suggest the original reports of APOL1 in proximal tubules likely reflects antibody non-specificity. As such, APOL1 expression in podocytes and endothelia should remain the focus for mechanistic studies in the APOL1-mediated kidney diseases.
Natalya A Blessing, Zhenzhen Wu, Sethu M Madhavan, Jonathan W Choy, Michelle Chen, Myung K Shin, Maarten Hoek, John R Sedor, John F O'Toole, Leslie A Bruggeman
1414 related Products with: Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.0.2 mL100 μg100 μg500 200 100 μg100 μg100 μg100uL100 μg100.00 ug
#33767059 // To Up
Apolipoprotein L1 and mechanisms of kidney disease susceptibility.Allelic variants in the gene for apolipoprotein L1 (APOL1), found only in individuals of African ancestry, explain a majority of the excess risk of kidney disease in African Americans. However, a clear understanding how the disease-associated APOL1 variants cause kidney injury and the identity of environmental stressors that trigger the injury process have not been determined.
Leslie A Bruggeman, John R Sedor, John F O'Toole5mg540 tests10mg500ug500
#33576823 2021/02/12 To Up
The spectrum of kidney biopsies in hospitalized patients with COVID-19, acute kidney injury, and/or proteinuria.We report a multicentric retrospective case series of patients with COVID-19 who developed acute kidney injury and/or proteinuria and underwent a kidney biopsy in the Paris and its metropolitan area. Forty-seven patients (80.9% men) with COVID-19 who underwent a kidney biopsy between March 08 and May 19, 2020 were included. Median age was 63 years IQR [52-69]. Comorbidities included hypertension (66.0%), diabetes mellitus (27.7%), obesity (27.7%), history of chronic kidney (25.5%), cardiac (38.6%) and respiratory (27.3%) diseases. Initial symptoms were fever (85.1%), cough (63.8%), shortness of breath (55.3%), and diarrhea (23.4%). Almost all patients developed acute kidney injury (97.9%) and 63.8% required renal replacement therapy. Kidney biopsy showed two main histopathological patterns, including acute tubular injury in 20 (42.6%) patients, and glomerular injury consisting of collapsing glomerulopathy and focal segmental glomerulosclerosis in 17 (36.2%) patients. Two (4.3%) patients had acute vascular nephropathy, while eight (17%) had alternative diagnosis most likely unrelated to COVID-19. Acute tubular injury occurred almost invariably in the setting of severe forms of COVID-19, whereas patients with glomerular injury had various profiles of COVID-19 severity and collapsing glomerulopathy was only observed in patients harboring a combination of APOL1 risk variants. At last follow-up, 16 of the 30 patients who initially required dialysis were still on dialysis, and 9 died. The present study describes the spectrum of kidney lesions in patients with COVID-19. While acute tubular injury is correlated with COVID-19 severity, the pattern of glomerular injury is intimately associated with the expression of APOL1 risk variants.
Sophie Ferlicot, Matthieu Jamme, FranÃ§ois Gaillard, Julie Oniszczuk, Aymeric Couturier, Olivia May, Anne GrÃ¼nenwald, AurÃ©lie Sannier, Anissa Moktefi, OphÃ©lie Le Monnier, Camille Petit-Hoang, Nadine Maroun, Albane Brodin-Sartorius, Arthur Michon, HÃ©lÃ¨ne Dobosziewicz, Fabrizio Andreelli, Matthieu Guillet, Hassane Izzedine, Christian Richard, Manon Dekeyser, Romain Arrestier, Thomas SthelÃ©, Edouard LefÃ¨vre, Alexis Mathian, Christophe Legendre, Charlotte Mussini, Marie-Christine Verpont, Nicolas Pallet, Zahir Amoura, Marie Essig, Renaud Snanoudj, Isabelle Brocheriou-Spelle, HÃ©lÃ¨ne FranÃ§ois, Xavier Belenfant, Guillaume Geri, Eric Daugas, Vincent Audard, David Buob, Ziad A Massy, Mohamad Zaidan,
1583 related Products with: The spectrum of kidney biopsies in hospitalized patients with COVID-19, acute kidney injury, and/or proteinuria.96T
#33119586 2020/10/29 To Up
Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG).
Precil D Neves, Ramaiane A Bridi, JanaÃna A Ramalho, LectÃcia B Jorge, Elieser H Watanabe, Andreia Watanabe, Luis Yu, Viktoria Woronik, Rafaela B Pinheiro, Leonardo A Testagrossa, LÃvia B Cavalcante, Denise M Malheiros, Cristiane B Dias, Luiz F Onuchic
1657 related Products with: Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.400Tests1 kit1 kit20 96 assays 100 assays1 kit(96 Wells)100 assays1 kit100
#32889430 2020/08/20 To Up
The Trypanosoma Brucei KIFC1 Kinesin Ensures the Fast Antibody Clearance Required for Parasite Infectivity.Human innate immunity to Trypanosoma brucei involves the trypanosome C-terminal kinesin TbKIFC1, which transports internalized trypanolytic factor apolipoprotein L1 (APOL1) within the parasite. We show that TbKIFC1 preferentially associates with cholesterol-containing membranes and is indispensable for mammalian infectivity. Knockdown of TbKIFC1 did not affect trypanosome growth inÂ vitro but rendered the parasites unable to infect mice unless antibody synthesis was compromised. Surface clearance of Variant Surface Glycoprotein (VSG)-antibody complexes was far slower in these cells, which were more susceptible to capture by macrophages. This phenotype was not due to defects in VSG expression or trafficking but to decreased VSG mobility in a less fluid, stiffer surface membrane. This change can be attributed to increased cholesterol level in the surface membrane in TbKIFC1 knockdown cells. Clearance of surface-bound antibodies by T.Â brucei is therefore essential for infectivity and depends on high membrane fluidity maintained by the cholesterol-trafficking activity of TbKIFC1.
Laurence Lecordier, Sophie Uzureau, Gilles Vanwalleghem, Magali Deleu, Jean-Marc Crowet, Paul Barry, Barry Moran, Paul Voorheis, Andra-Cristina Dumitru, Yoshiki Yamaryo-BottÃ©, Marc Dieu, Patricia Tebabi, Benoit Vanhollebeke, Laurence Lins, Cyrille Y BottÃ©, David Alsteens, Yves DufrÃªne, David PÃ©rez-Morga, Derek P Nolan, Etienne Pays
1552 related Products with: The Trypanosoma Brucei KIFC1 Kinesin Ensures the Fast Antibody Clearance Required for Parasite Infectivity.100ul
#32764142 2020/08/06 To Up
Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.APOL1 is found in human kidney podocytes and endothelia. Variants G1 and G2 of the gene account for the high frequency of nondiabetic CKD among African Americans. Proposed mechanisms of kidney podocyte cytotoxicity resulting from variant overexpression implicate different subcellular compartments. It is unclear where endogenous podocyte APOL1 resides, because previous immunolocalization studies utilized overexpressed protein or commercially available antibodies that crossreact with APOL2. This study describes and distinguishes the locations of both APOLs.
Suzie J Scales, Nidhi Gupta, Ann M De MaziÃ¨re, George Posthuma, Cecilia P Chiu, Andrew A Pierce, Kathy HÃ¶tzel, Jianhua Tao, Oded Foreman, Georgios Koukos, Francesca Oltrabella, Judith Klumperman, WeiYu Lin, Andrew S Peterson
1436 related Products with: Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box2 Pieces/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box
#32764138 2020/08/06 To Up
Domain-Specific Antibodies Reveal Differences in the Membrane Topologies of Apolipoprotein L1 in Serum and Podocytes.Circulating APOL1 lyses trypanosomes, protecting against human sleeping sickness. Two common African gene variants of , G1 and G2, protect against infection by species of trypanosomes that resist wild-type APOL1. At the same time, the protection predisposes humans to CKD, an elegant example of balanced polymorphism. However, the exact mechanism of APOL1-mediated podocyte damage is not clear, including APOL1's subcellular localization, topology, and whether the damage is related to trypanolysis.
Nidhi Gupta, Xinhua Wang, Xiaohui Wen, Paul Moran, Maciej Paluch, Philip E Hass, Amy Heidersbach, Benjamin Haley, Daniel Kirchhofer, Randall J Brezski, Andrew S Peterson, Suzie J Scales
1621 related Products with: Domain-Specific Antibodies Reveal Differences in the Membrane Topologies of Apolipoprotein L1 in Serum and Podocytes.4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box4 Membranes/Box
#32668317 2020/07/12 To Up
COVID-19-Related Collapsing Glomerulopathy in a Kidney Transplant Recipient.We report a case of a kidney transplant recipient who presented with acute kidney injury and nephrotic-range proteinuria in a context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Kidney biopsy revealed collapsing glomerulopathy. Droplet-based digital polymerase chain reaction did not detect the presence of SARS-CoV-2 RNA in the biopsy fragment, and the virus was barely detectable in plasma at the time of the biopsy. SARS-CoV-2 RNAemia peaked several days later, followed by a seroconversion despite the absence of circulating CD19-positive lymphocytes at admission due to rituximab-based treatment of antibody-mediated rejection 3 months earlier. Genotyping for the 2 risk alleles of the apolipoprotein L1 (APOL1) gene revealed that the donor carried the low-risk G0/G2 genotype. This case illustrates that coronavirus disease 2019 infection may promote a collapsing glomerulopathy in kidney allografts with a low-risk APOL1 genotype in the absence of detectable SARS-CoV-2 RNA in the kidney and that podocyte injury may precede SARS-CoV-2 RNAemia.
HÃ©lÃ¨ne Lazareth, HÃ©lÃ¨ne PÃ©rÃ©, Yannick Binois, Melchior Chabannes, Juliet Schurder, Thomas Bruneau, Alexandre Karras, Eric Thervet, Marion Rabant, David Veyer, Nicolas Pallet
1453 related Products with: COVID-19-Related Collapsing Glomerulopathy in a Kidney Transplant Recipient.2 Pieces/Box2 Pieces/Box
#32621069 2020/07/03 To Up
Rapid progression to end-stage renal disease in a child with IgA-dominant infection-related glomerulonephritis associated with parvovirus B19.Parvovirus B19 (PVB19) has been known to cause acute glomerulonephritis and nephrotic syndrome with various renal histologic patterns, such as endocapillary glomerulonephritis and collapsing glomerulopathy. Remission is achieved spontaneously or by treatment with steroid and/or immunosuppressants in most patients, except those with sickle cell anemia or two APOL1 risk alleles. In this study, we report the case of a previously healthy 5-year-old boy with infection-related glomerulonephritis (IRGN) associated with PVB19 that progressed to end-stage renal disease (ESRD). He presented with macrohematuria, nephrotic-range proteinuria, and progressive renal dysfunction despite treatment with methylprednisolone pulse therapy, plasmapheresis, and intravenous immunoglobulin. The kidney biopsy specimens exhibited endocapillary infiltration and mesangiolysis with cellular crescent formation. Immunofluorescence analysis revealed that IgA was dominantly positive in the glomeruli, with some co-localized with KM55, which is a specific monoclonal antibody for galactose-deficient IgA1 (Gd-IgA1). The intensity of the KM55 signal in the present patient was weaker than that in patients with IgA nephropathy. To our knowledge, this is the first report of IRGN associated with PVB19 that progressed to ESRD without any underlying diseases. Further investigations are needed to determine the significance of IgA and Gd-IgA1 deposition in IRGN associated with PVB19.
Yoko Shirai, Kenichiro Miura, Tomoo Yabuuchi, Takeshi Nagasawa, Kiyonobu Ishizuka, Kazuhiro Takahashi, Sekiko Taneda, Kazuho Honda, Yutaka Yamaguchi, Hitoshi Suzuki, Yusuke Suzuki, Motoshi Hattori
2841 related Products with: Rapid progression to end-stage renal disease in a child with IgA-dominant infection-related glomerulonephritis associated with parvovirus B19.100
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia