GH ACTION Headlines Sat Dec 14 08:44:32 UTC 2024

data/AOPWikiRDF-Void.ttl

@@ -10,29 +10,29 @@
 @prefix freq:  <http://purl.org/cld/freq/> .
 :AOPWikiRDF.ttl	a	void:Dataset ;
 	dc:description	"AOP-Wiki RDF data from the AOP-Wiki database" ;
-	pav:createdOn	"2024-12-07"^^xsd:date;
-	dcterms:modified	"2024-12-07"^^xsd:date ;
-	pav:createdWith	"aop-wiki-xml-2024-12-07", :Promapping ;
+	pav:createdOn	"2024-12-14"^^xsd:date;
+	dcterms:modified	"2024-12-14"^^xsd:date ;
+	pav:createdWith	"aop-wiki-xml-2024-12-14", :Promapping ;
 	pav:createdBy	<https://zenodo.org/badge/latestdoi/146466058> ;
 	foaf:homepage	<https://aopwiki.org> ;
 	dcterms:accuralPeriodicity  freq:quarterly ;
-	dcat:downloadURL	<https://aopwiki.org/downloads/aop-wiki-xml-2024-12-07> .
+	dcat:downloadURL	<https://aopwiki.org/downloads/aop-wiki-xml-2024-12-14> .
 
 :AOPWikiRDF-Genes.ttl	a	void:Dataset ;
 	dc:description	"AOP-Wiki RDF extension with gene mappings based on approved names and symbols" ;
-	pav:createdOn	"2024-12-07 08:53:14.788988" ;
-	pav:createdWith	"aop-wiki-xml-2024-12-07", :HGNCgenes ;
+	pav:createdOn	"2024-12-14 08:44:31.032820" ;
+	pav:createdWith	"aop-wiki-xml-2024-12-14", :HGNCgenes ;
 	pav:createdBy	<https://zenodo.org/badge/latestdoi/146466058> ;
 	dcterms:accuralPeriodicity  freq:quarterly ;
 	foaf:homepage	<https://aopwiki.org> ;
-	dcat:downloadURL	<https://aopwiki.org/downloads/aop-wiki-xml-2024-12-07>, <https://www.genenames.org/download/custom/> . 
+	dcat:downloadURL	<https://aopwiki.org/downloads/aop-wiki-xml-2024-12-14>, <https://www.genenames.org/download/custom/> . 
 
 :HGNCgenes.txt	a	void:Dataset, void:Linkset ;
 	dc:description	"HGNC approved symbols and names for genes" ;
 	dcat:downloadURL	<https://www.genenames.org/download/custom/> ;
-	pav:importedOn	"Sat Dec  7 08:24:06 2024" .
+	pav:importedOn	"Sat Dec 14 08:23:51 2024" .
 
 <https://proconsortium.org/download/current/promapping.txt>	a	void:Dataset, void:Linkset;
 	dc:description	"PRotein ontology mappings to protein database identifiers";
 	dcat:downloadURL	<https://proconsortium.org/download/current/promapping.txt>;
-	pav:importedOn	"Sat Dec  7 08:29:28 2024".
+	pav:importedOn	"Sat Dec 14 08:27:27 2024".

data/AOPWikiRDF.ttl

@@ -67655,8 +67655,8 @@ aop.events:1690
 	rdfs:label	"KE 1690" ;
 	foaf:page	<https://identifiers.org/aop.events/1690> ;
 	rdfs:seeAlso	<https://identifiers.org/aop.events/1690> ;
-	dc:title	"Decrease, testosterone levels " ;
-	dcterms:alternative	"Decrease, testosterone levels" ;
+	dc:title	"Decrease, circulating testosterone levels " ;
+	dcterms:alternative	"Decrease, circulating testosterone levels" ;
 	dc:source	"AOPWiki" ;
 	dc:description	"""Testosterone is an endogenous steroid hormone and a potent androgen. Androgens act by binding androgen receptors in androgen-responsive tissues (Murashima et al., 2015). Testosterone and other androgens such as dihydrotestosterone (DHT) are important for reproductive development and masculinization of the fetus.&nbsp;Androgens are also important for bone, brain, muscle and skin health (Alemany, 2022). Just like other steroid hormones, testosterone is produced through a process known as steroidogenesis which is controlled by enzymes converting cholesterol into all of the downstream steroid hormones.&nbsp;In steroidogenesis, androstenedione or androstenediol is converted to testosterone by the enzymes 17&beta;-hydroxysteroid dehydrogenase (HSD) or 3&beta;-HSD, respectively. Testosterone can then be converted to the more potent androgen, DHT, by 5&alpha;-reductase, or aromatized by aromatase (CYP19A1) into estrogens.&nbsp;Testosterone secreted in blood circulation can be found free but more frequently is found bound to SHBG or albumin (Trost &amp; Mulhall, 2016). 
 
@@ -75082,7 +75082,7 @@ Progression through the cycle is dependent on sufficient nutrient availability t
 
 Various protein complexes, known as cyclins, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors (CKIs) regulate passage through each phase by activating and inhibiting specific processes (Lovicu et al., 2014). The CDKs are responsible for controlling progression through the cell cycle. They promote DNA synthesis and mitosis, and therefore cell division (Barnum &amp; O&rsquo;Connell, 2014). Furthermore, growth factors are required to stimulate cell division, but after passing through the restriction point at G1 they are no longer necessary (Lovicu et al., 2014).&nbsp;&nbsp;
 
-In the context of cancer, one hallmark is the sustained and uncontrolled cell proliferation (Hanahan et al., 2011, Portt et al., 2011). When cells obtain a growth advantage due to mutations in critical genes that regulate cell cycle progression, they may begin to proliferate excessively, resulting in hyperplasia and potentially leading to the development of a tumor. This is often achieved through oncogene activation and inactivation of tumor suppressor genes (Hanahan et al., 2011). Cell inactivation and the replacement of these cells can initiate clonal expansion (Heidenreich adn Paretzke et al., 2008).&nbsp;
+In the context of cancer, one hallmark is the sustained and uncontrolled cell proliferation (Hanahan et al., 2011, Portt et al., 2011). When cells obtain a growth advantage due to mutations in critical genes that regulate cell cycle progression, they may begin to proliferate excessively, resulting in hyperplasia and potentially leading to the development of a tumor. This is often achieved through oncogene activation and inactivation of tumor suppressor genes (Hanahan et al., 2011). Cell inactivation and the replacement of these cells can initiate clonal expansion (Heidenreich and Paretzke et al., 2008).&nbsp;
 
 Sustained atrophy/degeneration olfactory epithelium under the influence of a cytotoxic agent leads to adaptive tissue remodeling. Cell types unique to olfactory epithelium, e.g. olfactory neurons, sustentacular cells and Bowmans glands, are replaced by cell types comprising respiratory epithelium or squamous epithelium.
 """ ;
@@ -82688,6 +82688,7 @@ OECD defines clastogens as &lsquo;any substance that causes structural chromosom
 	pato:0000047	"Unspecific" ;
 	aopo:LifeStageContext	"All life stages" ;
 	ncbitaxon:131567	"WCS_9606",ncbitaxon:10116,ncbitaxon:10090 ;
+	go:0008150	go:0031052 ;
 	pato:0000001	"WIKI:1" ;
 	pato:0001241	go:0005694 ;
 	dcterms:isPartOf	aop:272,aop:296,aop:478 .
@@ -98525,7 +98526,7 @@ Upon gluten ingestion, proteolytic fragments are generated through enzymatic cle
 	aopo:CellTypeContext	cl:0000451 ;
 	aopo:OrganContext	uberon:0002114 ;
 	go:0008150	vt:0001835 ;
-	pato:0000001	"WIKI:1" ;
+	pato:0000001	"WIKI:3" ;
 	pato:0001241	fma:84795 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -98557,7 +98558,7 @@ aop.events:2253
 	aopo:CellTypeContext	cl:0000084 ;
 	aopo:OrganContext	uberon:0002370 ;
 	go:0008150	go:0035822 ;
-	pato:0000001	"WIKI:1" ;
+	pato:0000001	"WIKI:3" ;
 	pato:0001241	go:0042105 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -98583,7 +98584,7 @@ For the antibody-mediated recognition of deamidated gluten and TG2, B cell recep
 	aopo:CellTypeContext	cl:0000236 ;
 	aopo:OrganContext	uberon:0002371 ;
 	go:0008150	go:0002206 ;
-	pato:0000001	"WIKI:1" ;
+	pato:0000001	"WIKI:3" ;
 	pato:0001241	go:0019815 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -98606,7 +98607,7 @@ Additionally, infections can cause molecular mimicry, where pathogen-derived ant
 	nci:C25664	"""Cellular""" ;
 	aopo:OrganContext	uberon:0002108 ;
 	go:0008150	go:0002376 ;
-	pato:0000001	"WIKI:1" ;
+	pato:0000001	"WIKI:3" ;
 	dcterms:isPartOf	aop:524 .
 
 aop.events:2256
@@ -98638,8 +98639,8 @@ In healthy individuals, autoreactive B cells are controlled through receptor edi
 	ncbitaxon:131567	"WCS_9606" ;
 	aopo:CellTypeContext	cl:0000236 ;
 	aopo:OrganContext	uberon:0010394 ;
-	go:0008150	go:0002263 ;
-	pato:0000001	"WIKI:1" ;
+	go:0008150	go:0002312 ;
+	pato:0000001	"WIKI:3" ;
 	pato:0001241	cl:0000236 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -98652,11 +98653,11 @@ aop.events:2260
 	dc:title	"Gluten-reactive CD4+ T cells, activation" ;
 	dcterms:alternative	"Activation of gluten-reactive CD4+ T cells" ;
 	dc:source	"AOPWiki" ;
-	dc:description	"""In the intestinal mucosa of celiac disease patients, gluten-specific CD4+ T cells recognize gliadin antigens, particularly those deamidated by the tissue transglutaminase enzyme (TG2). These antigens are presented by antigen-presenting cells (APCs) expressing HLA-DQ2 or HLA-DQ8 molecules. Antigen presentation activates the gluten-specific CD4+ T cells, initiating a cascade of immune responses.
+	dc:description	"""In the intestinal mucosa of celiac disease patients, gluten-specific CD4+ T cells recognize gliadin antigens, particularly those deamidated by the tissue transglutaminase enzyme (TG2) (Lundin et al., 1993; Arentz-Hansen et al., 2000). These antigens are presented by antigen-presenting cells (APCs) expressing HLA-DQ2 or HLA-DQ8 molecules (Arentz-Hansen et al., 2000; Broughton et al., 2012). Antigen presentation activates the gluten-specific CD4+ T cells, initiating a cascade of immune responses.
 
-Upon activation, gluten-specific CD4+ T cells undergo rapid clonal expansion and differentiation into a pro-inflammatory population that secretes cytokines such as interferon-gamma (IFN&gamma;) and tumor necrosis factor-alpha (TNF&alpha;). Additionally, B cells with B cell receptors (BCRs) specific for TG2-gliadin complexes can present these complexes to gluten-specific CD4+ T cells, further stimulating their activation.
+Upon activation, gluten-specific CD4+ T cells undergo rapid clonal expansion and differentiation into a pro-inflammatory population that secretes cytokines such as interferon-gamma (IFN&gamma;) and tumor necrosis factor-alpha (TNF&alpha;) (Nilsen et al., 1998). Additionally, B cells with B cell receptors (BCRs) specific for TG2-gliadin complexes can present these complexes to gluten-specific CD4+ T cells, further stimulating their activation (Di Niro et al., 2012).
 
-The release of IFN&gamma; upregulates the expression of HLA class II molecules on APCs, enhancing the efficiency of gluten peptide presentation. This creates a feedback loop that amplifies antigen presentation and intensifies the T cell-mediated immune response to gluten.
+The release of IFN&gamma; upregulates the expression of HLA class II molecules on APCs, enhancing the efficiency of gluten peptide presentation (Meresse et al., 2006). This creates a feedback loop that amplifies antigen presentation and intensifies the T cell-mediated immune response to gluten.
 """ ;
 	mmo:0000000	"""
 	Isolation from Intestinal Biopsies: Gluten-reactive T cells can be isolated from patients with celiac disease but not from healthy controls.
@@ -98674,7 +98675,7 @@ The release of IFN&gamma; upregulates the expression of HLA class II molecules o
 	aopo:CellTypeContext	cl:0000084 ;
 	aopo:OrganContext	uberon:0015834 ;
 	go:0008150	go:0002286 ;
-	pato:0000001	"WIKI:1" ;
+	pato:0000001	"WIKI:3" ;
 	pato:0001241	cl:0000084 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -98691,7 +98692,7 @@ aop.events:2275
 	aopo:CellTypeContext	cl:0000084 ;
 	aopo:OrganContext	uberon:0015834 ;
 	go:0008150	go:0072678,go:0036336 ;
-	pato:0000001	"WIKI:1","WIKI:1" ;
+	pato:0000001	"WIKI:3","WIKI:3" ;
 	pato:0001241	cl:0000084,cl:0000145 ;
 	dcterms:isPartOf	aop:524 .
 
@@ -99353,6 +99354,73 @@ aop.events:2270
 	dc:description	"""
 
 Cholesterol has a variety of roles in organisms, including as a cellular membrane component that helps maintain structure and fluidity, and a precursor for steroid hormones (Sakakura et al. 2001; Horton et al. 2003; Howe et al. 2017). &nbsp;The cholesterol synthesis pathway involves a number of precursor molecules and enzymes (Sakakura et al. 2001; Itkonen et al. 2023).
+
+Table 1: List of cholesterol synthesis enzymes with identifier of enzyme (Uniprot, 2024).
+
+
+
+
+			Enzyme
+			Identifier
+
+
+			Hydroxymethylglutaryl-CoA synthase
+			EC:2.3.3.10
+
+
+			Hydroxymethylglutaryl-CoA reductase
+			EC:1.1.1.34
+
+
+			Mevalonate kinase
+			EC:2.7.1.36
+
+
+			Phosphomevalonate kinase
+			EC:2.7.4.2
+
+
+			Diphosphomevalonate decarboxylase
+			EC:4.1.1.33
+
+
+			Isopentenyl-diphosphate Delta-isomerase
+			EC:5.3.3.2
+
+
+			Geranylgeranyl diphosphate synthase
+			EC 2.5.1.29
+
+
+			(2E,6E)-farnesyl diphosphate synthase
+			EC:2.5.1.10
+
+
+			Squalene synthase
+			EC:2.5.1.21
+
+
+			Squalene monooxygenase
+			EC:1.14.14.17
+
+
+			Lanosterol synthase
+			EC:5.4.99.7
+
+
+			Sterol 14alpha-demethylase
+			EC:1.14.14.154
+
+
+			Delta(7)-sterol 5(6)-desaturase
+			EC:1.14.19.20
+
+
+			7-dehydrocholesterol reductase
+			EC:1.3.1.21
+
+
+
 """ ;
 	mmo:0000000	"""Cholesterol synthesis enyzmes are measured by changes in gene expression (via real time PCR; Sakakura et al. 2001; Horton et al. 2003; Howe et al. 2017)) and protein (via Western blotting or enzyme immunoassays) levels (Karpale et al. 2021). &nbsp;
 """ ;
@@ -175109,6 +175177,11 @@ go:0005391	a	go:0008150 ;
 	dc:title	"sodium:potassium-exchanging ATPase activity" ;
 	dc:source	"GO" . 
 
+go:0031052	a	go:0008150 ;
+	dc:identifier	go:0031052 ;
+	dc:title	"chromosome breakage" ;
+	dc:source	"GO" . 
+
 go:0004908	a	go:0008150 ;
 	dc:identifier	go:0004908 ;
 	dc:title	"interleukin-1 receptor activity" ;
@@ -175184,11 +175257,6 @@ go:0042769	a	go:0008150 ;
 	dc:title	"DNA damage response, detection of DNA damage" ;
 	dc:source	"GO" . 
 
-go:0031052	a	go:0008150 ;
-	dc:identifier	go:0031052 ;
-	dc:title	"chromosome breakage" ;
-	dc:source	"GO" . 
-
 mp:0008866	a	go:0008150 ;
 	dc:identifier	mp:0008866 ;
 	dc:title	"chromosomal instability" ;
@@ -175784,6 +175852,11 @@ go:0002376	a	go:0008150 ;
 	dc:title	"immune system process" ;
 	dc:source	"GO" . 
 
+go:0002312	a	go:0008150 ;
+	dc:identifier	go:0002312 ;
+	dc:title	"B cell activation involved in immune response" ;
+	dc:source	"GO" . 
+
 hp:0002608	a	go:0008150 ;
 	dc:identifier	hp:0002608 ;
 	dc:title	"Celiac disease" ;