From 432c94fbb23832bd651c503f52547b7deb4e654a Mon Sep 17 00:00:00 2001
From: Liliana Sanfilippo <liliana.sanfilippo@uni-bielefeld.de>
Date: Sun, 29 Sep 2024 14:36:05 +0200
Subject: [PATCH] bib formatting

---
 src/components/makeSources.tsx     |  2 +-
 src/sources/mattij-inv-sources.tsx | 43 ++++++++++++++++++++++++++++--
 2 files changed, 42 insertions(+), 3 deletions(-)

diff --git a/src/components/makeSources.tsx b/src/components/makeSources.tsx
index 2a313b78..fff600a2 100644
--- a/src/components/makeSources.tsx
+++ b/src/components/makeSources.tsx
@@ -73,7 +73,7 @@ export const BibtexParser: React.FC<BibtexParserProps> = ({ bibtexSources , spec
       //console.log("All parsed entries: ", allEntries);
     } catch (error) {
      // console.error("Error parsing BibTeX: ", error);
-      alert("An error occurred while parsing the BibTeX entries. Please check the format.");
+      alert("An error occurred while parsing the BibTeX entries. Please check the format." + bibtexSources);
     }
   }, [bibtexSources]);
 
diff --git a/src/sources/mattij-inv-sources.tsx b/src/sources/mattij-inv-sources.tsx
index 44e384c1..1efed740 100644
--- a/src/sources/mattij-inv-sources.tsx
+++ b/src/sources/mattij-inv-sources.tsx
@@ -10,7 +10,46 @@ export default function MattijsInterviewSources(){
 
 
 const bibtexSources = [
-    ` 
+    `
+    @article{Bulcaen_Kortleven_Liu_Maule_Dreano_Kelly_Ensinck_Thierie_Smits_Ciciani_et,
+	title        = {
+		Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in
+		human organoids and airway epithelial cells
+	},
+	author       = {
+		Bulcaen, Mattijs and Kortleven, Phéline and Liu, Ronald B. and Maule, Giulia
+		and Dreano, Elise and Kelly, Mairead and Ensinck, Marjolein M. and Thierie,
+		Sam and Smits, Maxime and Ciciani, Matteo and Hatton, Aurelie and Chevalier,
+		Benoit and Ramalho, Anabela S. and Casadevall i Solvas, Xavier and Debyser,
+		Zeger and Vermeulen, François and Gijsbers, Rik and Sermet-Gaudelus, Isabelle
+		and Cereseto, Anna and Carlon, Marianne S.
+	},
+	year         = 2024,
+	month        = may,
+	journal      = {Cell Reports Medicine},
+	pages        = 101544,
+	doi          = {10.1016/j.xcrm.2024.101544},
+	issn         = {2666-3791},
+	abstractnote = {
+		Prime editing is a recent, CRISPR-derived genome editing technology capable
+		of introducing precise nucleotide substitutions, insertions, and deletions.
+		Here, we present prime editing approaches to correct L227R- and N1303K-CFTR,
+		two mutations that cause cystic fibrosis and are not eligible for current
+		market-approved modulator therapies. We show that, upon DNA correction of the
+		CFTR gene, the complex glycosylation, localization, and, most importantly,
+		function of the CFTR protein are restored in HEK293T and 16HBE cell lines.
+		These findings were subsequently validated in patient-derived rectal
+		organoids and human nasal epithelial cells. Through analysis of predicted and
+		experimentally identified candidate off-target sites in primary stem cells,
+		we confirm previous reports on the high prime editor (PE) specificity and its
+		potential for a curative CF gene editing therapy. To facilitate future
+		screening of genetic strategies in a translational CF model, a machine
+		learning algorithm was developed for dynamic quantification of CFTR function
+		in organoids (DETECTOR: “detection of targeted editing of CFTR in
+		organoids”).
+	}
+}
+
+    `
 
-@article{Bulcaen_Kortleven_Liu_Maule_Dreano_Kelly_Ensinck_Thierie_Smits_Ciciani_et al._2024, title={Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in human organoids and airway epithelial cells}, ISSN={2666-3791}, DOI={10.1016/j.xcrm.2024.101544}, abstractNote={Prime editing is a recent, CRISPR-derived genome editing technology capable of introducing precise nucleotide substitutions, insertions, and deletions. Here, we present prime editing approaches to correct L227R- and N1303K-CFTR, two mutations that cause cystic fibrosis and are not eligible for current market-approved modulator therapies. We show that, upon DNA correction of the CFTR gene, the complex glycosylation, localization, and, most importantly, function of the CFTR protein are restored in HEK293T and 16HBE cell lines. These findings were subsequently validated in patient-derived rectal organoids and human nasal epithelial cells. Through analysis of predicted and experimentally identified candidate off-target sites in primary stem cells, we confirm previous reports on the high prime editor (PE) specificity and its potential for a curative CF gene editing therapy. To facilitate future screening of genetic strategies in a translational CF model, a machine learning algorithm was developed for dynamic quantification of CFTR function in organoids (DETECTOR: “detection of targeted editing of CFTR in organoids”).}, journal={Cell Reports Medicine}, author={Bulcaen, Mattijs and Kortleven, Phéline and Liu, Ronald B. and Maule, Giulia and Dreano, Elise and Kelly, Mairead and Ensinck, Marjolein M. and Thierie, Sam and Smits, Maxime and Ciciani, Matteo and Hatton, Aurelie and Chevalier, Benoit and Ramalho, Anabela S. and Casadevall i Solvas, Xavier and Debyser, Zeger and Vermeulen, François and Gijsbers, Rik and Sermet-Gaudelus, Isabelle and Cereseto, Anna and Carlon, Marianne S.}, year={2024}, month=may, pages={101544} } `
 ]
\ No newline at end of file
-- 
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