Kerem Fidan
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View article: Pirin Transcriptionally Regulates PLA2G4A To Inhibit Ferroptosis in Colorectal Cancer via Lipid Profile Remodeling
Pirin Transcriptionally Regulates PLA2G4A To Inhibit Ferroptosis in Colorectal Cancer via Lipid Profile Remodeling Open
Ferroptosis, an iron‐dependent cell death driven by lipid peroxidation, is a promising therapeutic target in colorectal cancer (CRC); however, its regulation remains unclear. Here, Pirin (PIR) is recognized as a ferroptosis suppressor that…
View article: Supplementary Figure S8 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S8 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Role of Iron-(Fe3+) and Pirin in CRC
View article: Supplementary Figure S3 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S3 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
ITDRF-CETSA method identifying SP2509’s target.
View article: Supplementary Tables from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Tables from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Supplementary Table S1: List of all the candidates from ITDRF-MS along with their function other than Pirin (second column shows the UniProt ID (protein accession number), third column shows gene ID, fourth column shows full protein name, …
View article: Supplementary Figure S4 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S4 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Iron-(Fe3+) bound to Pirin positively regulates hTERT
View article: Supplementary Figure S10 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S10 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
SP2509 mediated inhibition of CRCs occurs due to loss of iron-(Fe3+) mediated Pirin activity
View article: Supplementary Figure S11 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S11 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
SP2509’s inhibitory action is specific to CRC specifically to CMS3 subtype
View article: Supplementary Figure S1 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S1 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Validation of reporter cell lines for small molecule screens.
View article: Supplementary Figure S6 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S6 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
SP2509 competes with Iron-(Fe3+) bound to Pirin
View article: Supplementary Figure S9 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S9 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Role of Iron-(Fe3+) and Pirin in CRC
View article: Supplementary Figure S5 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S5 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
SP2509 mediated regulation of TERT through Pirin
View article: Supplementary Figure S2 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S2 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Effect of LSD1 on hTERT expression and telomerase activity.
View article: Data from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Data from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Over-consumption of iron-rich red meat and hereditary or genetic iron overload are associated with an increased risk of colorectal carcinogenesis, yet the mechanistic basis of how metal-mediated signaling leads to oncogenesis remains enigm…
View article: Supplementary Figure S12 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S12 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Regulation of Sp1 and FBXW7 levels by Pirin and SP2509
View article: Supplementary Figure S13 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S13 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Iron-(Fe3+) regulates hTERT via Pirin-mediated control of FBXW7, the Sp1 targeting E3 ligase
View article: Supplementary Figure S7 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Supplementary Figure S7 from Iron-(Fe<sup>3+</sup>)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
SP2509 interaction with Iron-(Fe3+)
View article: Iron-(Fe3+)-Dependent Reactivation of Telomerase Drives Colorectal Cancers
Iron-(Fe3+)-Dependent Reactivation of Telomerase Drives Colorectal Cancers Open
Over-consumption of iron-rich red meat and hereditary or genetic iron overload are associated with an increased risk of colorectal carcinogenesis, yet the mechanistic basis of how metal-mediated signaling leads to oncogenesis remains enigm…
View article: Non-canonical roles of canonical telomere binding proteins in cancers
Non-canonical roles of canonical telomere binding proteins in cancers Open
Reactivation of telomerase is a major hallmark observed in 90% of all cancers. Yet paradoxically, enhanced telomerase activity does not correlate with telomere length and cancers often possess short telomeres; suggestive of supplementary n…