Results 11 to 20 of about 7,139 (201)

Structural features and oligomeric nature of human podocin domain

Biochemistry and Biophysics Reports, 2020
Podocytes are crucial cells of the glomerular filtration unit and plays a vital role at the interface of the blood-urine barrier. Podocyte slit-diaphragm is a modified tight junction that facilitates size and charge-dependent permselectivity.
Sandeep K.N. Mulukala, Shivkumar S. Irukuvajjula, Krishan Kumar, Kanchan Garai, Pannuru Venkatesu, Ramakrishna Vadrevu, Anil K. Pasupulati   +6 more
doaj   +3 more sources

An inducible mouse model of podocin-mutation-related nephrotic syndrome. [PDF]

PLoS ONE, 2017
Mutations in the NPHS2 gene, encoding podocin, cause hereditary nephrotic syndrome. The most common podocin mutation, R138Q, is associated with early disease onset and rapid progression to end-stage renal disease. Knock-in mice carrying a R140Q mutation,
Mansoureh Tabatabaeifar, Tanja Wlodkowski, Ivana Simic, Helga Denc, Geraldine Mollet, Stefanie Weber, John Julius Moyers, Barbara Brühl, Michael Joseph Randles, Rachel Lennon, Corinne Antignac, Franz Schaefer   +11 more
doaj   +5 more sources

Early detection of active glomerular lesions in dogs and cats using podocin [PDF]

Journal of Veterinary Research, 2019
In veterinary medicine, sensitive and specific markers of the early stages of renal failure still remain to be established. Podocytes could be a promising diagnostic tool in veterinary nephrology, especially in the differentiation of active pathological ...
Szczepankiewicz Barbara, Pasławska Urszula, Nowak Marcin, Bąchor Remigiusz, Czyżewska-Buczyńska Agnieszka, Pasławski Robert, Szewczuk Zbigniew   +6 more
doaj   +3 more sources

A Rare NPHS2 Mutation (E130K) in Hereditary Steroid-Resistant Nephrotic Syndrome: A Case Report. [PDF]

Case Rep Nephrol
Hereditary steroid‐resistant nephrotic syndrome (HSRNS) due to mutations in the NPHS2 gene (encoding podocin) is a rare genetic condition that typically presents in childhood. We report a case of a 2‐year‐and‐8‐month‐old male, the seventh child of consanguineous parents, who presented with recurrent fever, febrile tonic‐clonic seizures, and periorbital
Mujahed RH, Salloum OH, Ishreiteh NF, Hosheyh HM, Hashem ADA, Shamestti YF, Hroub MR.   +6 more
europepmc   +2 more sources

A membranous nephropathy variant mimicking minimal change disease. [PDF]

J Pathol Clin Res
Abstract This study characterizes a novel disease pattern of membranous nephropathy (MN) that exhibits overlapping clinicopathological features with minimal change disease (MCD), termed ‘MCD‐like MN’. Patients with histologically confirmed MN showing sparse and segmental subepithelial electron‐dense deposits (EDD) but clinically resembling MCD were ...
Pan C, Xiang S, Jiang M, Li Y, Huang B, Ye T, Du Y, Tang X, Yuan Y.   +8 more
europepmc   +2 more sources

Cdk5 Contributes to Diabetic Islet β Cell and Kidney Injury by Impairing Autophagy. [PDF]

FASEB J
Over‐activation of cyclin‐dependent kinase 5 (Cdk5) is involved in the development of diabetes and its complications. Mechanistically, Cdk5 expression was upregulated in diabetic mice, which induced attenuated autophagy and increased apoptosis of islet β cells, as well as decreased insulin secretion.
Tao Y, Wang L, Liu Y, Wei Y, Wang R, Sha S, Zheng S, Hou S, Liu S.   +8 more
europepmc   +2 more sources

TRPC6 effects on albumin permeation, nephrin shedding, and apoptosis in podocytes: Role of calcineurin and metalloproteases. [PDF]

Physiol Rep
Certain ligands of pattern recognition receptors can induce a rapid increase in albumin permeability across a podocyte monolayer that can be seen in 1 h, but activation of TRPC6 for up to 24 h does not mimick this process. However, continuous TRPC6 activation for 24 h results in nephrin ectodomain shedding that calcineurin activation and ...
Kim EY, Dryer SE.
europepmc   +2 more sources

Proteolytic cleavage of Podocin by Matriptase exacerbates podocyte injury [PDF]

Journal of Biological Chemistry, 2020
Podocyte injury is a critical step toward the progression of renal disease and is often associated with a loss of slit diaphragm proteins, including Podocin. Although there is a possibility that the extracellular domain of these slit diaphragm proteins can be a target for a pathological proteolysis, the precise mechanism driving the phenomenon remains ...
Shota Ozawa, Masaya Matsubayashi, Hitoki Nanaura, Motoko Yanagita, Kiyoshi Mori, Katsuhiko Asanuma, Nobuyuki Kajiwara, Kazuyuki Hayashi, Hiroshi Ohashi, Masato Kasahara, Hideki Yokoi, Hiroaki Kataoka, Eiichiro Mori, Takahiko Nakagawa   +13 more
openaire   +2 more sources

In silico Structural characterization of podocin and assessment of nephrotic syndrome‐associated podocin mutants [PDF]

IUBMB Life, 2016
AbstractNephrotic syndrome (NS) is manifested by hyperproteinuria, hypoalbuminemia, and edema. NPHS2 that encodes podocin was found to have most mutations among the genes that are involved in the pathophysiology of NS. Podocin, an integral membrane protein belonging to stomatin family, is expressed exclusively in podocytes and is localized to slit ...
Mulukala, Sandeep Kumar Narasimha, Nishad, Rajkishor, Kolligundla, Lakshmi Prasanna, Saleem, Moin A., Prabhu, Nagu Prakash, Pasupulati, Anil Kumar   +5 more
openaire   +4 more sources

Interaction with Podocin Facilitates Nephrin Signaling [PDF]

Journal of Biological Chemistry, 2001
Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes ...
Huber, Tobias B., Köttgen, Michael, Schilling, Birgit, Walz, Gerd, Benzing, Thomas   +4 more
openaire   +3 more sources