Update tsv, md and png files

_data/WP5200-bibliography.tsv

@@ -1,4 +1,5 @@
 ID	Database	Citation
+9412493	Pubmed	"Interaction of muscle and brain sodium channels with multiple members of the syntrophin family of dystrophin-associated proteins. Gee SH, Madhavan R, Levinson SR, Caldwell JH, Sealock R, Froehner SC. J Neurosci. 1998 Jan 1;18(1):128–37.  <a href=""http://www.ncbi.nlm.nih.gov/pubmed/9412493"" target=""_blank"" class=""external"" rel=""nofollow"">PubMed</a> <a href=""https://europepmc.org/abstract/MED/9412493"" target=""_blank"" class=""external"" rel=""nofollow"">Europe PMC</a> <a href=""https://scholia.toolforge.org/pubmed/9412493"" target=""_blank"" class=""external"" rel=""nofollow"">Scholia</a>"
 15077147	Pubmed	"Mitogen-activated protein kinases in apoptosis regulation. Wada T, Penninger JM. Oncogene. 2004 Apr 12;23(16):2838–49.  <a href=""http://www.ncbi.nlm.nih.gov/pubmed/15077147"" target=""_blank"" class=""external"" rel=""nofollow"">PubMed</a> <a href=""https://europepmc.org/abstract/MED/15077147"" target=""_blank"" class=""external"" rel=""nofollow"">Europe PMC</a> <a href=""https://scholia.toolforge.org/pubmed/15077147"" target=""_blank"" class=""external"" rel=""nofollow"">Scholia</a>"
 15102918	Pubmed	"Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture. Chen C, Westenbroek RE, Xu X, Edwards CA, Sorenson DR, Chen Y, et al. J Neurosci. 2004 Apr 21;24(16):4030–42.  <a href=""http://www.ncbi.nlm.nih.gov/pubmed/15102918"" target=""_blank"" class=""external"" rel=""nofollow"">PubMed</a> <a href=""https://europepmc.org/abstract/MED/15102918"" target=""_blank"" class=""external"" rel=""nofollow"">Europe PMC</a> <a href=""https://scholia.toolforge.org/pubmed/15102918"" target=""_blank"" class=""external"" rel=""nofollow"">Scholia</a>"
 17442248	Pubmed	"Interdependence of PKC-dependent and PKC-independent pathways for presynaptic plasticity. Wierda KDB, Toonen RFG, de Wit H, Brussaard AB, Verhage M. Neuron. 2007 Apr 19;54(2):275–90.  <a href=""http://www.ncbi.nlm.nih.gov/pubmed/17442248"" target=""_blank"" class=""external"" rel=""nofollow"">PubMed</a> <a href=""https://europepmc.org/abstract/MED/17442248"" target=""_blank"" class=""external"" rel=""nofollow"">Europe PMC</a> <a href=""https://scholia.toolforge.org/pubmed/17442248"" target=""_blank"" class=""external"" rel=""nofollow"">Scholia</a>"

_data/WP5200-datanodes.tsv

@@ -4,6 +4,7 @@ Ca2+	Metabolite	chebi:29108	""					wikidata:Q23905776	chebi:29108	inchikey:BHPQY
 GABA	Metabolite	chebi:16865	""					wikidata:Q106345483;wikidata:Q210021	chebi:16865;chebi:59888	inchikey:BTCSSZJGUNDROE-UHFFFAOYSA-N	pubchem.compound:6992099;pubchem.compound:119	chemspider:116	hmdb:HMDB0000112	kegg.compound:C00334	lipidmaps:LMFA01100039
 Syntaxin	Metabolite	wikidata:Q390407	""												
 Na+	Metabolite	chebi:29101	""					wikidata:Q3154110	chebi:29101	inchikey:FKNQFGJONOIPTF-UHFFFAOYSA-N	pubchem.compound:923	chemspider:899	hmdb:HMDB0000588	kegg.compound:C01330	
+SNTA1	GeneProduct	ensembl:ENSG00000101400	"Guides the positioning of Nav1.1 on the membrane"	ensembl:ENSG00000101400	ncbigene:6640	hgnc.symbol:SNTA1	uniprot:Q13424								
 SCN1A	GeneProduct	ensembl:ENSG00000144285	""	ensembl:ENSG00000144285	ncbigene:6323	hgnc.symbol:SCN1A	uniprot:A0A286YFA8;uniprot:A0A286YEQ8;uniprot:A0A1B0GWE6;uniprot:A0A5F9ZHI6;uniprot:A0A1B0GVX7;uniprot:A0A1B0GUX7;uniprot:A0A1W2PPJ3;uniprot:A0A1B0GUN7;uniprot:P35498;uniprot:A0A286YF26								
 PRR5L	Protein	uniprot:Q6MZQ0	""	ensembl:ENSG00000135362	ncbigene:79899	hgnc.symbol:PRR5L	uniprot:E9PJV4;uniprot:E9PL62;uniprot:E9PLJ6;uniprot:E9PS02;uniprot:E9PP62;uniprot:Q6MZQ0;uniprot:E9PP25;uniprot:E9PIU0								
 PRKCA	Protein	uniprot:P17252	""	ensembl:ENSG00000154229	ncbigene:5578	hgnc.symbol:PRKCA	uniprot:J3KN97;uniprot:L7RSM7;uniprot:P17252;uniprot:J3KRN5								

_pathways/WP5200.md

@@ -4,22 +4,22 @@ annotations:
   parent: animal cell
   type: Cell Type Ontology
   value: neuron
-- id: CL:0000598
-  parent: animal cell
-  type: Cell Type Ontology
-  value: pyramidal neuron
 - id: DOID:0080422
   parent: genetic disease
   type: Disease Ontology
   value: Dravet syndrome
-- id: CL:0011005
-  parent: animal cell
-  type: Cell Type Ontology
-  value: GABAergic interneuron
 - id: PW:0000013
   parent: disease pathway
   type: Pathway Ontology
   value: disease pathway
+- id: CL:0011005
+  parent: animal cell
+  type: Cell Type Ontology
+  value: GABAergic interneuron
+- id: CL:0000598
+  parent: animal cell
+  type: Cell Type Ontology
+  value: pyramidal neuron
 authors:
 - MiriamBabukhian
 - Leadoerner
@@ -31,21 +31,21 @@ citedin: ''
 communities:
 - RareDiseases
 description: 'Dravet syndrome is a rare form of epilepsy. Between 70% and 80% of patients
-  carry sodium channel α1 subunit gene (SCN1A) loss of function mutations. Truncating
+  carry sodium channel α1 subunit gene (SCN1A) loss of function mutations. Truncating
   mutations (early stop codon) account for about 40% and have a significant correlation
   with an earlier age of seizures onset. The mutations lead to haploinsufficiency
-  of the voltage-gated sodium channel α subunit NaV1.1 in the of GABAergic inhibitory
+  of the voltage-gated sodium channel α subunit NaV1.1 in the of GABAergic inhibitory
   interneurons in the brain.  Mutations in other genes like KCNA1, CHD2, PCDH19 and
   STXBP1 can also lead to Dravet syndrome.  '
-last-edited: 2024-07-23
+last-edited: 2024-11-08
 ndex: null
 organisms:
 - Homo sapiens
 redirect_from:
 - /index.php/Pathway:WP5200
 - /instance/WP5200
-- /instance/WP5200_r134566
-revision: r134566
+- /instance/WP5200_r135747
+revision: r135747
 schema-jsonld:
 - '@context': https://schema.org/
   '@id': https://wikipathways.github.io/pathways/WP5200.html
@@ -54,10 +54,10 @@ schema-jsonld:
     '@type': Organization
     name: WikiPathways
   description: 'Dravet syndrome is a rare form of epilepsy. Between 70% and 80% of
-    patients carry sodium channel α1 subunit gene (SCN1A) loss of function mutations.
+    patients carry sodium channel α1 subunit gene (SCN1A) loss of function mutations.
     Truncating mutations (early stop codon) account for about 40% and have a significant
     correlation with an earlier age of seizures onset. The mutations lead to haploinsufficiency
-    of the voltage-gated sodium channel α subunit NaV1.1 in the of GABAergic inhibitory
+    of the voltage-gated sodium channel α subunit NaV1.1 in the of GABAergic inhibitory
     interneurons in the brain.  Mutations in other genes like KCNA1, CHD2, PCDH19
     and STXBP1 can also lead to Dravet syndrome.  '
   keywords:
@@ -92,6 +92,7 @@ schema-jsonld:
   - SCN2B
   - SCN3B
   - SCN4B
+  - SNTA1
   - STXBP1
   - Syntaxin
   - TNF