Tubular cell loss in early inv/nphp2 mutant kidneys represents a possible homeostatic mechanism in cortical tubular formation.

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Tubular cell loss in early inv/nphp2 mutant kidneys represents a possible homeostatic mechanism in cortical tubular formation.

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2018 nî lūn-bûn

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2018年の論文

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年學術文章

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2018年學術文章

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Tubular cell loss in early inv ...... in cortical tubular formation.

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Tubular cell loss in early inv ...... in cortical tubular formation.

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Tubular cell loss in early inv ...... in cortical tubular formation.

@en

Tubular cell loss in early inv ...... in cortical tubular formation.

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Tubular cell loss in early inv ...... in cortical tubular formation.

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Tubular cell loss in early inv ...... in cortical tubular formation.

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P1476

Tubular cell loss in early inv ...... in cortical tubular formation.

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P2093

Hirotaka Kanazawa

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Takahiko Yokoyama

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P2860

AIF promotes chromatinolysis and caspase-independent programmed necrosis by interacting with histone H2AX

Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination

Polycystin-2 localizes to kidney cilia and the ciliary level is elevated in orpk mice with polycystic kidney disease

The ciliary protein Nek8/Nphp9 acts downstream of Inv/Nphp2 during pronephros morphogenesis and left-right establishment in zebrafish

Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair

Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways

The polycystic kidney disease proteins, polycystin-1, polycystin-2, polaris, and cystin, are co-localized in renal cilia

Loss of oriented cell division does not initiate cyst formation

New insights into ADPKD molecular pathways using combination of SAGE and microarray technologies.

Multiorgan mRNA misexpression in murine autosomal recessive polycystic kidney disease.

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e0198580

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scholarly article

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10.1371/JOURNAL.PONE.0198580

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English

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P478

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Masaki Shigeta

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2018-06-11T00:00:00Z

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29889867

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P932

5995398

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