Lompat ke isi

Nefrin: Perbedaan antara revisi

Ensiklopedia Pengetahuan Universitas Islam Sultan Agung

Maintenance script (bicara | kontrib)

37.956 suntingan
Maintenance script (bicara | kontrib)
37.956 suntingan
Impor teks terkontrol dari Wikipedia bahasa Indonesia; revisi 26994147; atribusi sumber disertakan.
 
Maintenance script (bicara | kontrib)
37.956 suntingan
Presentation V4: sitasi, referensi, Math, Wikimedia Commons, dan atribusi
 
Baris 1: Baris 1:
'''Nefrin''' adalah [[glikoprotein]] transmembran dari golongan [[imunoglobulin]] hasil [[ekspresi gen|ekspresi]] [[gen]]etik [[NPHS1]] oleh [[podosit]], yang merupakan komponen struktural pada diafragma yang terdapat pada tiap celah di antara struktur deret [[podosit]]. Nefrin juga berfungsi sebagai [[molekul]] [[adhesi sel|adhesi]] antara [[protein]] seperti [[podosin]], [[CD2AP]], [[FAT-1]], [[Neph-1]], dengan membran podosit.
'''Nefrin''' adalah [[glikoprotein]] transmembran dari golongan [[imunoglobulin]] hasil [[ekspresi gen|ekspresi]] [[gen]]etik [[NPHS1]] oleh [[podosit]],<ref>[http://www.ncbi.nlm.nih.gov/pubmed/11865096 Expression of nephrin in acquired human glomerular disease]. ''Division of Nephrology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine; Huh W, Kim DJ, Kim MK, Kim YG, Oh HY, Ruotsalainen V, Tryggvason K''.</ref> yang merupakan komponen struktural pada diafragma yang terdapat pada tiap celah di antara struktur deret [[podosit]].<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2709686 Nck Proteins Maintain the Adult Glomerular Filtration Barrier]. ''Department of Molecular and Cellular Biology, University of Guelph, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Department of Molecular and Medical Genetics, Institute of Medical Science, University of Toronto, Department of Medicine, McGill University Health Centre, Epitomics, Inc, Burlingame, Division of Nephrology, St. Michael's Hospital; Nina Jones, Laura A. New, Megan A. Fortino, Vera Eremina, Julie Ruston, Ivan M. Blasutig, Lamine Aoudjit, Youling Zou, Xiuwen Liu, Guo-Liang Yu, Tomoko Takano, Susan E. Quaggin, dan Tony Pawson''.</ref> Nefrin juga berfungsi sebagai [[molekul]] [[adhesi sel|adhesi]] antara [[protein]] seperti [[podosin]], [[CD2AP]], [[FAT-1]], [[Neph-1]],<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659252 Phosphorylation of Nephrin Triggers Ca2+ Signaling by Recruitment and Activation of Phospholipase C-γ1]. ''Division of Cellular Proteomics (BML) and Department of Oncology, Institute of Medical Science, Department of Pediatrics, Graduate School of Medicine, University of Tokyo, Department of Anatomy, Juntendo University School of Medicine, Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Department of Biochemistry, School of Pharmaceutical Sciences, Kitasato University; Yutaka Harita, Hidetake Kurihara, Hidetaka Kosako, Tohru Tezuka, Takashi Sekine, Takashi Igarashi, Ikuroh Ohsawa, Shigeo Ohta, dan Seisuke Hattori''.</ref> dengan membran podosit.


Dari percobaan dengan menggunakan [[hewan]] [[tikus]], diketahui bahwa ekspresi nefrin pada podosit akan menghambat [[lintasan metabolisme|lintasan]] [[faktor transkripsi]] [[NF-κB]], sehingga defisiensi nefrin akan mengaktifkan lintasan tersebut dan berakibat menjadi [[glomerulosklerosis]], [[albuminuria|proteinuria]], dan [[edema]].
Dari percobaan dengan menggunakan [[hewan]] [[tikus]], diketahui bahwa ekspresi nefrin pada podosit akan menghambat [[lintasan metabolisme|lintasan]] [[faktor transkripsi]] [[NF-κB]],<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723981 Nephrin Deficiency Activates NF-κB and Promotes Glomerular Injury]. ''Molecular Medicine Unit, Institute of Child Health, Academic Renal Unit, University of Bristol, Southmead Hospital, Spanish National Cancer Research Centre, Department of Genome Science, Genome Research Institute, University of Cincinnati; Sagair Hussain, Leile Romio, Moin Saleem, Peter Mathieson, Manuel Serrano, Jorge Moscat, Maria Diaz-Meco, Peter Scambler, dan Ania Koziell''.</ref> sehingga defisiensi nefrin akan mengaktifkan lintasan tersebut dan berakibat menjadi [[glomerulosklerosis]], [[albuminuria|proteinuria]], dan [[edema]].<ref>[http://www.ncbi.nlm.nih.gov/pubmed/11136707 The murine nephrin gene is specifically expressed in kidney, brain and pancreas: inactivation of the gene leads to massive proteinuria and neonatal death]. ''Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet; Putaala H, Soininen R, Kilpeläinen P, Wartiovaara J, Tryggvason K''.</ref>
 
Ekspresi nefrin juga terdapat pada [[membran plasma]], [[vesikel]] [[insulin]], [[sel beta]] dan [[sel MIN-6]], dan dapat diinduksi dengan [[senyawa organik]] [[Doksisiklina]]. Kenaikan konsentrasi [[gula darah]] akan meningkatkan ekspresi nefrin pada sel beta dan sel MIN-6 sebelum terjadi [[sekresi]] [[insulin]], serta menginduksi [[endositosis]] nefrin pada [[podosit]]. Ekspresi nefrin menurun pada [[diabetes mellitus#diabetes mellitus tipe 2|diabetes tipe 2]] dan [[nefropati]].
 
== Rujukan ==


Ekspresi nefrin juga terdapat pada [[membran plasma]], [[vesikel]] [[insulin]], [[sel beta]] dan [[sel MIN-6]], dan dapat diinduksi dengan [[senyawa organik]] [[Doksisiklina]].<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797869 Inducible Nephrin Transgene Expression in Podocytes Rescues Nephrin-Deficient Mice from Perinatal Death]. ''Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Centre for Bioanalytical Sciences, Dublin City University, Department of Human Genetics, Leiden University Medical Center, Haartman Institute, Department of Pathology and Experimental Animal Centre, University of Helsinki, Clinical Institute of Pathology, Medical University Vienna; Juuso Juhila, Markus Lassila, Ramon Roozendaal, Eero Lehtonen, Marcel Messing, Brigitte Langer, Dontscho Kerjaschki, J. Sjef Verbeek, dan Harry Holthofer''.</ref> Kenaikan konsentrasi [[gula darah]] akan meningkatkan ekspresi nefrin pada sel beta dan sel MIN-6 sebelum terjadi [[sekresi]] [[insulin]], serta menginduksi [[endositosis]] nefrin pada [[podosit]]. Ekspresi nefrin menurun pada [[diabetes mellitus#diabetes mellitus tipe 2|diabetes tipe 2]] dan [[nefropati]].<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797921 Nephrin Is Expressed on the Surface of Insulin Vesicles and Facilitates Glucose-Stimulated Insulin Release]. ''Diabetes Research Institute, University of Miami L. Miller School of Medicine, Division of Nephrology and Hypertension–Miami Institute of Renal Medicine, Division of Molecular Medicine, University of Miami L. Miller School of Medicine, Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Policlinico San Matteo, Università degli Studi di Pavia, The Rolf Luft Research Center for Diabetes and Endocrinology, Cell Matrix Biology, Karolinska Institutet, Clinical Institute of Pathology, Medical University; Alessia Fornoni, Jongmin Jeon, Javier Varona Santos, Lorenzo Cobianchi, Alexandra Jauregui, Luca Inverardi, Slavena A. Mandic, Christina Bark, Kevin Johnson, George McNamara, Antonello Pileggi, R. Damaris Molano, Jochen Reiser, Karl Tryggvason, Dontscho Kerjaschki, Per-Olof Berggren, Peter Mundel, dan Camillo Ricordi''.</ref>


== Referensi ==
<references />


== Sumber dan atribusi ==
== Sumber dan atribusi ==


Konten artikel ini diadaptasi dari [https://id.wikipedia.org/w/index.php?title=Nefrin&oldid=26994147 Wikipedia bahasa Indonesia], revisi 26994147 (2025-03-04T16:52:11Z), yang tersedia berdasarkan lisensi Creative Commons Atribusi-BerbagiSerupa (CC BY-SA). Mohon gunakan konten ini secara bijak serta sesuai dengan ketentuan lisensi yang berlaku.
Konten artikel ini diadaptasi dari [https://id.wikipedia.org/w/index.php?title=Nefrin&oldid=26994147 Wikipedia bahasa Indonesia], revisi 26994147 (2025-03-04T16:52:11Z), yang tersedia berdasarkan lisensi Creative Commons Atribusi-BerbagiSerupa (CC BY-SA). Mohon gunakan konten ini secara bijak serta sesuai dengan ketentuan lisensi yang berlaku.
<!-- WIKI_UNISSULA_PRESENTATION_V4 -->

Revisi terkini sejak 29 Agustus 2026 13.59

Nefrin adalah glikoprotein transmembran dari golongan imunoglobulin hasil ekspresi genetik NPHS1 oleh podosit,[1] yang merupakan komponen struktural pada diafragma yang terdapat pada tiap celah di antara struktur deret podosit.[2] Nefrin juga berfungsi sebagai molekul adhesi antara protein seperti podosin, CD2AP, FAT-1, Neph-1,[3] dengan membran podosit.

Dari percobaan dengan menggunakan hewan tikus, diketahui bahwa ekspresi nefrin pada podosit akan menghambat lintasan faktor transkripsi NF-κB,[4] sehingga defisiensi nefrin akan mengaktifkan lintasan tersebut dan berakibat menjadi glomerulosklerosis, proteinuria, dan edema.[5]

Ekspresi nefrin juga terdapat pada membran plasma, vesikel insulin, sel beta dan sel MIN-6, dan dapat diinduksi dengan senyawa organik Doksisiklina.[6] Kenaikan konsentrasi gula darah akan meningkatkan ekspresi nefrin pada sel beta dan sel MIN-6 sebelum terjadi sekresi insulin, serta menginduksi endositosis nefrin pada podosit. Ekspresi nefrin menurun pada diabetes tipe 2 dan nefropati.[7]

Referensi

  1. ↑ Expression of nephrin in acquired human glomerular disease. Division of Nephrology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine; Huh W, Kim DJ, Kim MK, Kim YG, Oh HY, Ruotsalainen V, Tryggvason K.
  2. ↑ Nck Proteins Maintain the Adult Glomerular Filtration Barrier. Department of Molecular and Cellular Biology, University of Guelph, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Department of Molecular and Medical Genetics, Institute of Medical Science, University of Toronto, Department of Medicine, McGill University Health Centre, Epitomics, Inc, Burlingame, Division of Nephrology, St. Michael's Hospital; Nina Jones, Laura A. New, Megan A. Fortino, Vera Eremina, Julie Ruston, Ivan M. Blasutig, Lamine Aoudjit, Youling Zou, Xiuwen Liu, Guo-Liang Yu, Tomoko Takano, Susan E. Quaggin, dan Tony Pawson.
  3. ↑ Phosphorylation of Nephrin Triggers Ca2+ Signaling by Recruitment and Activation of Phospholipase C-γ1. Division of Cellular Proteomics (BML) and Department of Oncology, Institute of Medical Science, Department of Pediatrics, Graduate School of Medicine, University of Tokyo, Department of Anatomy, Juntendo University School of Medicine, Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Department of Biochemistry, School of Pharmaceutical Sciences, Kitasato University; Yutaka Harita, Hidetake Kurihara, Hidetaka Kosako, Tohru Tezuka, Takashi Sekine, Takashi Igarashi, Ikuroh Ohsawa, Shigeo Ohta, dan Seisuke Hattori.
  4. ↑ Nephrin Deficiency Activates NF-κB and Promotes Glomerular Injury. Molecular Medicine Unit, Institute of Child Health, Academic Renal Unit, University of Bristol, Southmead Hospital, Spanish National Cancer Research Centre, Department of Genome Science, Genome Research Institute, University of Cincinnati; Sagair Hussain, Leile Romio, Moin Saleem, Peter Mathieson, Manuel Serrano, Jorge Moscat, Maria Diaz-Meco, Peter Scambler, dan Ania Koziell.
  5. ↑ The murine nephrin gene is specifically expressed in kidney, brain and pancreas: inactivation of the gene leads to massive proteinuria and neonatal death. Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet; Putaala H, Soininen R, Kilpeläinen P, Wartiovaara J, Tryggvason K.
  6. ↑ Inducible Nephrin Transgene Expression in Podocytes Rescues Nephrin-Deficient Mice from Perinatal Death. Haartman Institute, Department of Bacteriology and Immunology, University of Helsinki, Centre for Bioanalytical Sciences, Dublin City University, Department of Human Genetics, Leiden University Medical Center, Haartman Institute, Department of Pathology and Experimental Animal Centre, University of Helsinki, Clinical Institute of Pathology, Medical University Vienna; Juuso Juhila, Markus Lassila, Ramon Roozendaal, Eero Lehtonen, Marcel Messing, Brigitte Langer, Dontscho Kerjaschki, J. Sjef Verbeek, dan Harry Holthofer.
  7. ↑ Nephrin Is Expressed on the Surface of Insulin Vesicles and Facilitates Glucose-Stimulated Insulin Release. Diabetes Research Institute, University of Miami L. Miller School of Medicine, Division of Nephrology and Hypertension–Miami Institute of Renal Medicine, Division of Molecular Medicine, University of Miami L. Miller School of Medicine, Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Policlinico San Matteo, Università degli Studi di Pavia, The Rolf Luft Research Center for Diabetes and Endocrinology, Cell Matrix Biology, Karolinska Institutet, Clinical Institute of Pathology, Medical University; Alessia Fornoni, Jongmin Jeon, Javier Varona Santos, Lorenzo Cobianchi, Alexandra Jauregui, Luca Inverardi, Slavena A. Mandic, Christina Bark, Kevin Johnson, George McNamara, Antonello Pileggi, R. Damaris Molano, Jochen Reiser, Karl Tryggvason, Dontscho Kerjaschki, Per-Olof Berggren, Peter Mundel, dan Camillo Ricordi.

Sumber dan atribusi

Konten artikel ini diadaptasi dari Wikipedia bahasa Indonesia, revisi 26994147 (2025-03-04T16:52:11Z), yang tersedia berdasarkan lisensi Creative Commons Atribusi-BerbagiSerupa (CC BY-SA). Mohon gunakan konten ini secara bijak serta sesuai dengan ketentuan lisensi yang berlaku.


Diperoleh dari "https://wiki.unissula.ac.id/index.php?title=Nefrin&oldid=26551"