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Balajikarthick Subramanian on Muck Rack

Balajikarthick Subramanian

As seen in: Science Magazine, ASN Journals
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Articles

INF2 mutations cause kidney disease through a gain-of-function mechanism

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By Chris K. Folland, Marcos Quijal-Zamorano, Kathleen E. Mandt, Balajikarthick Subramanian
| Science Magazine Verified
Abstract Heterozygosity for inverted formin-2 (INF2) mutations causes focal segmental glomerulosclerosis (FSGS) with or without Charcot-Marie-Tooth disease. A key question is whether the disease is caused by gain-of-function effects on INF2 or loss of function (haploinsufficiency). Despite established roles in multiple cellular processes, neither INF2 knockout mice nor mice with a disease-associated point mutation display an evident kidney or neurologic phenotype.
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FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes

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By Balajikarthick Subramanian, Justin V. Chun, Chandra Perez-Gill, Paul Yan
| ASN Journals Verified
Background Mutations in the gene encoding inverted formin-2 (INF2), a member of the formin family of actin regulatory proteins, are among the most common causes of autosomal dominant FSGS. INF2 is regulated by interaction between its N-terminal diaphanous inhibitory domain (DID) and its C-terminal diaphanous autoregulatory domain (DAD).
Open in Who Shared Issue with article?

FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes

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By Justin V. Chun, Paul Yan, Balajikarthick Subramanian, Chandra Perez-Gill
| ASN Journals Verified
Background Mutations in the gene encoding inverted formin-2 (INF2), a member of the formin family of actin regulatory proteins, are among the most common causes of autosomal dominant FSGS. INF2 is regulated by interaction between its N-terminal diaphanous inhibitory domain (DID) and its C-terminal diaphanous autoregulatory domain (DAD).
Open in Who Shared Issue with article?
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