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150 related items for PubMed ID: 27977723

  • 1. Functional Validation of an Alpha-Actinin-4 Mutation as a Potential Cause of an Aggressive Presentation of Adolescent Focal Segmental Glomerulosclerosis: Implications for Genetic Testing.
    Feng D, Steinke JM, Krishnan R, Birrane G, Pollak MR.
    PLoS One; 2016; 11(12):e0167467. PubMed ID: 27977723
    [Abstract] [Full Text] [Related]

  • 2. Mutational and Biological Analysis of alpha-actinin-4 in focal segmental glomerulosclerosis.
    Weins A, Kenlan P, Herbert S, Le TC, Villegas I, Kaplan BS, Appel GB, Pollak MR.
    J Am Soc Nephrol; 2005 Dec; 16(12):3694-701. PubMed ID: 16251236
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  • 3. Focal and segmental glomerulosclerosis in mice with podocyte-specific expression of mutant alpha-actinin-4.
    Michaud JL, Lemieux LI, Dubé M, Vanderhyden BC, Robertson SJ, Kennedy CR.
    J Am Soc Nephrol; 2003 May; 14(5):1200-11. PubMed ID: 12707390
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  • 5. Screening of ACTN4 and TRPC6 mutations in a Chinese cohort of patients with adult-onset familial focal segmental glomerulosclerosis.
    Zhang Q, Ma J, Xie J, Wang Z, Zhu B, Hao X, Yang L, Ren H, Chen N.
    Contrib Nephrol; 2013 May; 181():91-100. PubMed ID: 23689571
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  • 6. Familial focal segmental glomerulosclerosis associated with an ACTN4 mutation and paternal germline mosaicism.
    Choi HJ, Lee BH, Cho HY, Moon KC, Ha IS, Nagata M, Choi Y, Cheong HI.
    Am J Kidney Dis; 2008 May; 51(5):834-8. PubMed ID: 18436095
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  • 7. Focal segmental glomerulosclerosis ACTN4 mutants binding to actin: regulation by phosphomimetic mutations.
    Shao H, Wingert B, Weins A, Pollak MR, Camacho C, Wells A.
    Sci Rep; 2019 Oct 29; 9(1):15517. PubMed ID: 31664084
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  • 9. Analysis of mutations in alpha-actinin 4 and podocin genes of patients with chronic renal failure due to sporadic focal segmental glomerulosclerosis.
    Komatsuda A, Wakui H, Maki N, Kigawa A, Goto H, Ohtani H, Hamai K, Oyama Y, Makoto H, Sawada K, Imai H.
    Ren Fail; 2003 Jan 29; 25(1):87-93. PubMed ID: 12617336
    [Abstract] [Full Text] [Related]

  • 10. Three-layered proteomic characterization of a novel ACTN4 mutation unravels its pathogenic potential in FSGS.
    Bartram MP, Habbig S, Pahmeyer C, Höhne M, Weber LT, Thiele H, Altmüller J, Kottoor N, Wenzel A, Krueger M, Schermer B, Benzing T, Rinschen MM, Beck BB.
    Hum Mol Genet; 2016 Mar 15; 25(6):1152-64. PubMed ID: 26740551
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  • 11. Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis.
    Kaplan JM, Kim SH, North KN, Rennke H, Correia LA, Tong HQ, Mathis BJ, Rodríguez-Pérez JC, Allen PG, Beggs AH, Pollak MR.
    Nat Genet; 2000 Mar 15; 24(3):251-6. PubMed ID: 10700177
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  • 12. ACTN4 gene mutations and single nucleotide polymorphisms in idiopathic focal segmental glomerulosclerosis.
    Dai S, Wang Z, Pan X, Chen X, Wang W, Ren H, Feng Q, He JC, Han B, Chen N.
    Nephron Clin Pract; 2009 Mar 15; 111(2):c87-94. PubMed ID: 19142020
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  • 14. Mutational analysis of ACTN4, encoding α-actinin 4, in patients with focal segmental glomerulosclerosis using HRM method.
    Safaříková M, Reiterová J, Safránková H, Stekrová J, Zidková A, Obeidová L, Kohoutová M, Tesař V.
    Folia Biol (Praha); 2013 Mar 15; 59(3):110-5. PubMed ID: 23890478
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  • 16. Patients with ACTN4 mutations demonstrate distinctive features of glomerular injury.
    Henderson JM, Alexander MP, Pollak MR.
    J Am Soc Nephrol; 2009 May 15; 20(5):961-8. PubMed ID: 19357256
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  • 17. Alpha-actinin-4-mediated FSGS: an inherited kidney disease caused by an aggregated and rapidly degraded cytoskeletal protein.
    Yao J, Le TC, Kos CH, Henderson JM, Allen PG, Denker BM, Pollak MR.
    PLoS Biol; 2004 Jun 15; 2(6):e167. PubMed ID: 15208719
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  • 18. Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis.
    Read NC, Gutsol A, Holterman CE, Carter A, Coulombe J, Gray DA, Kennedy CR.
    Biochim Biophys Acta; 2014 Jul 15; 1842(7):1028-40. PubMed ID: 24662305
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  • 19. α-Actinin 4 potentiates nuclear factor κ-light-chain-enhancer of activated B-cell (NF-κB) activity in podocytes independent of its cytoplasmic actin binding function.
    Zhao X, Hsu KS, Lim JH, Bruggeman LA, Kao HY.
    J Biol Chem; 2015 Jan 02; 290(1):338-49. PubMed ID: 25411248
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  • 20. Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch.
    Feng D, Notbohm J, Benjamin A, He S, Wang M, Ang LH, Bantawa M, Bouzid M, Del Gado E, Krishnan R, Pollak MR.
    Proc Natl Acad Sci U S A; 2018 Feb 13; 115(7):1517-1522. PubMed ID: 29378953
    [Abstract] [Full Text] [Related]

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