about
Evidence for an interaction of the metalloprotease-disintegrin tumour necrosis factor alpha convertase (TACE) with mitotic arrest deficient 2 (MAD2), and of the metalloprotease-disintegrin MDC9 with a novel MAD2-related protein, MAD2betaEvidence for regulation of the tumor necrosis factor alpha-convertase (TACE) by protein-tyrosine phosphatase PTPH1Clustered arrangement of winged helix genes fkh-6 and MFH-1: possible implications for mesoderm developmentTRPC6 in glomerular health and disease: what we know and what we believeMetalloprotease-disintegrins: modular proteins capable of promoting cell-cell interactions and triggering signals by protein-ectodomain shedding.Exome sequencing and in vitro studies identified podocalyxin as a candidate gene for focal and segmental glomerulosclerosis.Rho activation of mDia formins is modulated by an interaction with inverted formin 2 (INF2)GLCCI1 single nucleotide polymorphisms in pediatric nephrotic syndrome.APOL1 kidney disease risk variants cause cytotoxicity by depleting cellular potassium and inducing stress-activated protein kinases.Inverted formin 2 regulates actin dynamics by antagonizing Rho/diaphanous-related formin signaling.Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2)TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription.Functional genetic variation in aminopeptidase A (ENPEP): lack of clear association with focal and segmental glomerulosclerosis (FSGS).How many Achilles' heels does a podocyte have? An update on podocyte biology.Intracellular maturation and localization of the tumour necrosis factor alpha convertase (TACE)Mice with mutant Inf2 show impaired podocyte and slit diaphragm integrity in response to protamine-induced kidney injuryTRPC6 and kidney disease: sclerosing more than just glomeruli?Nephrin AKTs on actin: The slit diaphragm-actin cytoskeleton signaling network expands.The Glomerular Disease Study and Trial Consortium: A Grassroots Initiative to Foster Collaboration and Innovation.Electrolyte abnormalities and progressive renal failure in a cancer patientTransmembrane insertases and N-glycosylation critically determine synthesis, trafficking, and activity of the nonselective cation channel TRPC6Small Molecule Targets TMED9 and Promotes Lysosomal Degradation to Reverse ProteinopathyCosmc-dependent mucin-type O-linked glycosylation is essential for podocyte function
P50
Q22010696-9A929A4E-D43B-40AE-B8DD-D135D6C5FC7FQ24305944-A01299CF-3696-4D53-BF79-ED77E6A510EEQ24336043-C088FBEA-5F6F-4F45-B164-13543CA63DE8Q24652809-7B8A6E57-8B79-4863-BCBE-21B90EF9B22AQ33752819-F1EAB74A-4E95-469E-B168-8FC1FAFA8D59Q33796482-344E6444-6CBE-44EC-B5CD-E2B13FF092EEQ34582764-46714433-6F05-4133-9AB3-0EE68BDBACD6Q36129301-39185487-B70A-4B1F-A2FF-6EB789119900Q36551655-5C7301EC-955A-4675-9592-52A22A093103Q36880430-724D204E-0098-4980-9075-14895092861FQ36947844-B5C2E81D-3F4F-4319-BA24-217165837402Q37139035-24DFA860-0A5A-4E77-9274-BAA0A660EC40Q37250921-EC5045A6-D79D-41F3-8D3B-B0DEBC9D17CAQ38217483-2566869A-D64A-495F-A05B-F643DFDD84ACQ40892360-42AA71AE-071F-4E31-A8D7-3D9034B800ACQ41825141-8D9D6CE4-8A45-4239-9D92-28EE917061A5Q52781359-EFB0D155-17BD-4216-9CC3-C3ED49A72245Q53498232-FE8C98AB-1BAE-4699-9D86-B6464AB178B7Q64917411-56CB8238-881E-4621-B577-9CFD8C323881Q79857237-B53267BC-3DEB-422E-A6E9-A888FC9EEE52Q91563348-16A190CB-7D44-46DC-899D-1D063B73292BQ92204301-7600A3F7-CAC4-4ECC-93E4-DC8B19D7341BQ92432773-33206687-6A95-472E-B7F7-059F3D54A2D9
P50
description
researcher
@en
name
Johannes Schlöndorff
@en
Schlöndorff J
@nl
type
label
Johannes Schlöndorff
@en
Schlöndorff J
@nl
altLabel
Schlöndorff J
@en
prefLabel
Johannes Schlöndorff
@en
Schlöndorff J
@nl
P106
P31
P496
0000-0002-9973-9731