Literature DB >> 17868089

Floxed allele for conditional inactivation of the voltage-gated sodium channel beta1 subunit Scn1b.

Chunling Chen1, Travis L Dickendesher, Fumitaka Oyama, Haruko Miyazaki, Nobuyuki Nukina, Lori L Isom.   

Abstract

The voltage-gated sodium channel gene Scn1b encodes the auxiliary subunit beta1, which is widely distributed in neurons and glia of the central and peripheral nervous systems, cardiac myocytes, skeletal muscle myocytes, and neuroendocrine cells. We showed previously that the Scn1b null mutation results in a complex and severe phenotype that includes retarded growth, seizures, ataxia, and death by postnatal day 21. We generated a floxed allele of Scn1b by inserting loxP sites surrounding the second coding exon. Ubiquitous deletion of the floxed exon by Cre recombinase using CMV-Cre-transgenic mice produced the Scn1b(del) allele. The null phenotype of Scn1b(del) homozygotes is indistinguishable from that of Scn1b nulls and confirms the invivo inactivation of Scn1b. Conditional inactivation ofthe floxed allele will make it possible to circumvent the lethality that results from complete loss of this gene, such that the physiological role of Scn1b in specific cell types and/or specific developmental time points can be investigated.

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Year:  2007        PMID: 17868089     DOI: 10.1002/dvg.20324

Source DB:  PubMed          Journal:  Genesis        ISSN: 1526-954X            Impact factor:   2.487


  8 in total

Review 1.  Sodium channel gene family: epilepsy mutations, gene interactions and modifier effects.

Authors:  Miriam H Meisler; Janelle E O'Brien; Lisa M Sharkey
Journal:  J Physiol       Date:  2010-03-29       Impact factor: 5.182

2.  Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.

Authors:  Xianming Lin; Heather O'Malley; Chunling Chen; David Auerbach; Monique Foster; Akshay Shekhar; Mingliang Zhang; William Coetzee; José Jalife; Glenn I Fishman; Lori Isom; Mario Delmar
Journal:  J Physiol       Date:  2014-09-17       Impact factor: 5.182

3.  A functional null mutation of SCN1B in a patient with Dravet syndrome.

Authors:  Gustavo A Patino; Lieve R F Claes; Luis F Lopez-Santiago; Emily A Slat; Raja S R Dondeti; Chunling Chen; Heather A O'Malley; Charles B B Gray; Haruko Miyazaki; Nobuyuki Nukina; Fumitaka Oyama; Peter De Jonghe; Lori L Isom
Journal:  J Neurosci       Date:  2009-08-26       Impact factor: 6.167

4.  Homozygous SCN1B variants causing early infantile epileptic encephalopathy 52 affect voltage-gated sodium channel function.

Authors:  Marcello Scala; Stephanie Efthymiou; Tipu Sultan; Jolien De Waele; Marta Panciroli; Vincenzo Salpietro; Reza Maroofian; Pasquale Striano; Filip Van Petegem; Henry Houlden; Frank Bosmans
Journal:  Epilepsia       Date:  2021-04-26       Impact factor: 6.740

Review 5.  Models and detection of spontaneous recurrent seizures in laboratory rodents.

Authors:  Bin Gu; Katherine A Dalton
Journal:  Zool Res       Date:  2017-07-18

6.  Scn1b deletion in adult mice results in seizures and SUDEP.

Authors:  Heather A O'Malley; Jacob M Hull; Brittany C Clawson; Chunling Chen; Gic Owens-Fiestan; Margaret B Jameson; Sara J Aton; Jack M Parent; Lori L Isom
Journal:  Ann Clin Transl Neurol       Date:  2019-05-08       Impact factor: 4.511

7.  Hippocampal µ-opioid receptors on GABAergic neurons mediate stress-induced impairment of memory retrieval.

Authors:  Mei-Mei Shi; Ka-Min Fan; Yan-Ning Qiao; Jin-Hui Xu; Li-Juan Qiu; Xiao Li; Ying Liu; Zhao-Qiang Qian; Chun-Ling Wei; Jing Han; Juan Fan; Ying-Fang Tian; Wei Ren; Zhi-Qiang Liu
Journal:  Mol Psychiatry       Date:  2019-05-29       Impact factor: 15.992

8.  Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.

Authors:  Jacob M Hull; Heather A O'Malley; Chunling Chen; Yukun Yuan; Nicholas Denomme; Alexandra A Bouza; Charles Anumonwo; Luis F Lopez-Santiago; Lori L Isom
Journal:  Ann Clin Transl Neurol       Date:  2020-09-26       Impact factor: 4.511

  8 in total

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