American Epilepsy Society (AES)
77^th Annual Meeting in Orlando, Fla. (Dec. 1-5, 2023)

• Cohen S, Smith L, Parthasarathy S, Bonkowski E, Hong W, Wiltrout K, et al. Voltage clamp and genetic variant pathogenicity: Epilepsy sodium channel variant curation expert panel consensus. Abstract No 3.356, 2023, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Epilepsy Society (AES)
75^th Annual Meeting in Chicago, Ill. (Dec. 3-7, 2021)

• Abreo T, Ji Z, Xu M, Dunbar C, Chavez A, Johnson J, et al. KCNQ2 G256W, a "moderate severity" developmental encephalopathy allele, modeled in silico, in vitro, and in knockin mice. Abstract No 1.118, 2021, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Academy of Neurology (AAN)
Virtual 2021 Annual Meeting (April 17-22, 2021)

• Cooper E, Joshi N, Millichap J, Tsuchida T, Nesbitt G, Taglialatela M, et al. The RIKEE database: Genotype-phenotype patterns in KCNQ channel related disease, based on 784 individuals and pedigrees. Neurology. 2021;96(15 Suppl):2427. 

American Epilepsy Society (AES)
73^rd Annual Meeting in Baltimore, Md. (Dec. 6-10, 2019)

• Ji Z-G, Moore O, Abreo T, Dworetzky S, Picchione KE, Cooper EC. KB-3061 is a potent activator of wild type KCNQ channels and restores current to KCNQ2 encephalopathy variants in vitro. Abstract No 3.047, 2019, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Epilepsy Society (AES)
72^nd Annual Meeting in New Orleans, La. (Nov. 30 - Dec. 4, 2018)

• Park S, Dunbar C, Tarkunde Y, Akbar A, Marks R, Lee M, et al. Pharmacodynamic dependence of retigabine on Kcnq2 expression in PV+ interneurons. Abstract No 3.053, 2018, American Epilepsy Society Annual Meeting, www.aesnet.org. 

Society for Neuroscience (SFN)
48^th Annual Meeting in San Diego, Calif. (Nov. 3-7, 2018)

• Zhang J, Chen C, Kim E, Procko E, Patel J, Choi R, et al. Missense epilepsy mutations in neuronal KCNQ/Kv7 channels occur at hotspots within highly conserved functional domains of Kv7.2 and Kv7.3. Program No. 558.12. 2018 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2018. Online. 

American Epilepsy Society (AES)
71^st Annual Meeting in Washington, DC (Dec. 1-5, 2017)

• Sands TT, Miceli F, Lesca G, Beck A, Cimino M, Strong N, et al. Autism with benzodiazepine-responsive electrical status epilepticus in sleep (ESES) caused by KCNQ3 gain-of-function variants. Abstract No 2.380, 2017, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Epilepsy Society (AES)
70^th Annual Meeting in Houston, Texas (Dec. 2-6, 2016)

• Ji Z, Tran B, Li L, Xu M, Cooper E. Functional characterization of three de novo KCNQ2 encephalopathy variants in the pore helix and responses to SF0034 and ICA-069673. Abstract No 3.256, 2016, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Joshi N, Taglialatela M, Weckhuysen S, Nesbitt G, Cooper E. An informatics infrastructure for KCNQ2 encephalopathy research including a patient registry, database, curation platform, and website. Abstract No 3.329, 2016, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Taglialatela M, Millichap J, Miceli F, De Maria M, Keator C, Joshi N, et al. Infantile spasms and encephalopathy without preceding neonatal seizures caused by KCNQ2 R198Q, a gain-of-function variant. Abstract No 2.366, 2016, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Wang X, Li L, Xu M, Mays J, Joshi N, Cooper E. Genotype-phenotype relationships In KCNQ2 related epilepsy and encephalopathy caused by variants in the pore region. Abstract No 3.134, 2016, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Epilepsy Society (AES)
69^th Annual Meeting in Philadelphia, Penn. (Dec. 4-8, 2015)

• Joshi N, Cooper EC, Taglialatela M, Weckhuysen S. An international, curated KCNQ2 registry, database and website. Abstract No 1.308, 2015, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Li L, Cooper EC. KCNQ2 encephalopathy: Novel single amino acid deletion variants strongly suppress currents and are responsive to SF0034. Abstract No 1.346, 2015, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Millichap J, Miceli F, Tran B, Keator C, Joshi N, Virginia Soldovieri M, et al. KCNQ2 p.Arg198Gln, a gain-of-function variant presenting recurrently as West syndrome without preceding neonatal seizures. Abstract No 3.337, 2015, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Mulkey SB, Ben-Zeev B, Cooper EC, Cilio M. Novel clinical features of KCNQ2 encephalopathy associated with the gain-of-function variant, R201C. Abstract No 2.386, 2015, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Soldovieri M, Ambrosino P, De Maria M, Mosca I, Miceli F, Striano P, et al. Pharmacological rescue of KCNQ2 channels carrying early-onset epileptic encephalopathy mutations. Abstract No 3.018, 2015, American Epilepsy Society Annual Meeting, www.aesnet.org. 

Experimental Biology (EB)
2015 Annual Meeting in Boston, Mass. (March 28 - April 1, 2015)

• Xu M, Cooper E. Differential Ankyrin-G binding of voltage-gated sodium and KCNQ2/3 potassium channels is mediated by an overlapping N-terminal binding site. FASEB J. 2015;29:714.3 

American Epilepsy Society (AES)
68^th Annual Meeting in Seattle, Wash. (Dec. 5-9, 2014)

• Park K, Millichap J, Cooper E. KCNQ2-deficiency: Clinical spectrum of epilepsy, encephalopathy, and response to ezogabine. Abstract No 3.210, 2014, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Tran B, Xu M, Cooper E. A KCNQ2/3 mutation causing severe epilepsy disrupts channel targeting to the axon initial segment. Abstract No 3.017, 2014, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Epilepsy Society (AES)
67^th Annual Meeting in Washington, DC (Dec. 6-10, 2013)

• Li L, Tran B, Xu M, Millichap J, Porter B, Cooper E. Pore loop KCNQ2 mutations causing epileptic encephalopathy strongly suppress wild type KCNQ2 currents when co-expressed in mammalian cells. Abstract No 3.022, 2013, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Tran B, Xu M, Cooper E. KCNQ2 targeting to the axon initial segment is disrupted in a mutant form causing severe epilepsy. Abstract No 1.022, 2013, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Xu M, Cooper E. Ankyrin-G as a potential molecular mechanism linking epilepsy and comorbid mood disorder. Abstract No 1.029, 2013, American Epilepsy Society Annual Meeting, www.aesnet.org. 

Society for Neuroscience (SFN)
43^rd Annual Meeting in San Diego, Calif. (Nov. 9-13, 2013)

• Chang K-J, Zollinger DR, Susuki K, Ho TS, Cooper EC, Bennett V, et al. Paranodal ankyrins: Enigmatic glial anchors. Program No. 699.05. 2013 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2013. Online. 
• Ho T, Zollinger DR, Xu M, Cooper EC, Stankewich MC, Bennett V, et al. The roles of ankyrin-G in node of Ranvier formation in vivo. Program No. 699.17. 2013 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2013. Online. 

American Epilepsy Society (AES)
66^th Annual Meeting in San Diego, Calif. (Nov. 30 - Dec. 4, 2012)

• Cooper EC, Carmant L, Flamini R, Kendall FD, Levisohn PM, Millichap JJ, et al. Clustering of mutations in a North American series supports a dominant-negative mechanism of KCNQ2 encephalopathy. Abstract No 1.354, 2012, American Epilepsy Society Annual Meeting, www.aesnet.org. 
• Millichap JJ, Levisohn PM, Tsuchida TN, Cooper EC. Treatment of KCNQ2 encephalopathy with ezogabine. Abstract No 1.355, 2012, American Epilepsy Society Annual Meeting, www.aesnet.org. 

American Academy of Neurology (AAN)
64^th Annual Meeting in New Orleans, La. (April 21-28, 2012)

• Cooper E. Ion channel modifications in epilepsy. Presented at the American Academy of Neurology (AAN), 64^th Annual Meeting in New Orleans, La. (April 21-28, 2012).