PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32557994-5	2020	Furthermore, we establish that the reaction order continues with 2-5$$-carbocyclization and 4$$-epimerization by the non-heme iron and 2-oxoglutarate-dependent enzymes SnoK and SnoN, respectively.	Heme	121-125	SKI like proto-oncogene	Homo sapiens	177-181
451491-5	1979	500 microgram/mlD-penicillamine added to skil cultures in vitro inhibited both collagen and general protein synthesis (p less than 0.01).	Penicillamine	18-31	SKI like proto-oncogene	Homo sapiens	41-45
32557994-5	2020	Furthermore, we establish that the reaction order continues with 2-5$$-carbocyclization and 4$$-epimerization by the non-heme iron and 2-oxoglutarate-dependent enzymes SnoK and SnoN, respectively.	Iron	126-130	SKI like proto-oncogene	Homo sapiens	177-181
32557994-5	2020	Furthermore, we establish that the reaction order continues with 2-5$$-carbocyclization and 4$$-epimerization by the non-heme iron and 2-oxoglutarate-dependent enzymes SnoK and SnoN, respectively.	Ketoglutaric Acids	135-149	SKI like proto-oncogene	Homo sapiens	177-181
31879190-9	2020	Collectively, our results demonstrate that SERCA2a gene transfer attenuates bleomycin (BLM)-induced PF by blocking the STAT3/FOXM1 pathway and promoting the SNON/SKI Axis.	Bleomycin	76-85	SKI like proto-oncogene	Homo sapiens	157-161
31876382-4	2020	The biosynthetic pathway of the anthracycline nogalamycin contains two such proteins, SnoK and SnoN, belonging to non-heme iron and 2-oxoglutarate-dependent mono-oxygenases.	Anthracyclines	32-57	SKI like proto-oncogene	Homo sapiens	95-99
31876382-4	2020	The biosynthetic pathway of the anthracycline nogalamycin contains two such proteins, SnoK and SnoN, belonging to non-heme iron and 2-oxoglutarate-dependent mono-oxygenases.	Heme	118-127	SKI like proto-oncogene	Homo sapiens	95-99
31876382-4	2020	The biosynthetic pathway of the anthracycline nogalamycin contains two such proteins, SnoK and SnoN, belonging to non-heme iron and 2-oxoglutarate-dependent mono-oxygenases.	2-oxoglutarate	132-146	SKI like proto-oncogene	Homo sapiens	95-99
31876382-5	2020	In spite of structural similarity, the two proteins catalyse distinct chemical reactions; SnoK is a C2-C5"" carbocyclase, whereas SnoN catalyses stereoinversion at the adjacent C4"" position.	Carbon	100-107	SKI like proto-oncogene	Homo sapiens	130-134
31876382-7	2020	Our analyses indicate that the carbocyclase SnoK is the ancestral form of the enzyme from which SnoN has evolved to catalyse stereoinversion at the neighboring carbon.	Carbon	160-166	SKI like proto-oncogene	Homo sapiens	96-100
32194108-5	2020	Importantly, the Snon-peak interrogates the continuous reduction of amorphous starch molecules during the aging, SAXS parameters including alpha and d describe starch ordered aggregate structures with larger scale than 2 nm are fitted well with pseudo Avrami equation.	Starch	78-84	SKI like proto-oncogene	Homo sapiens	17-21
32194108-5	2020	Importantly, the Snon-peak interrogates the continuous reduction of amorphous starch molecules during the aging, SAXS parameters including alpha and d describe starch ordered aggregate structures with larger scale than 2 nm are fitted well with pseudo Avrami equation.	Starch	160-166	SKI like proto-oncogene	Homo sapiens	17-21
31879190-9	2020	Collectively, our results demonstrate that SERCA2a gene transfer attenuates bleomycin (BLM)-induced PF by blocking the STAT3/FOXM1 pathway and promoting the SNON/SKI Axis.	Bleomycin	87-90	SKI like proto-oncogene	Homo sapiens	157-161
29709244-7	2018	Ajmaline-induced PVCs occurred more often in patients with non-missense mutations (Snon-missense) or missense mutations in transmembrane or pore regions of SCN5A-encoded channel protein (Smissense-TP) than patients with missense mutations in intra-/extracellular channel regions (Smissense-IE) and patients without SCN5A mutation (S-) (29%, 24%, 9%, and 3%, respectively; P<0.001).	Ajmaline	0-8	SKI like proto-oncogene	Homo sapiens	83-87
31028803-4	2019	KEY FINDINGS: Under the high-glucose condition, the activation of TGF-beta1/TAK1-induced phosphorylation and ubiquitination of SnoN protein resulted in reduced SnoN protein level as a consequence of enhanced SnoN degradation, which promoted EMT and ECM deposition in renal tubular epithelial cells.	Glucose	29-36	SKI like proto-oncogene	Homo sapiens	127-131
31028803-4	2019	KEY FINDINGS: Under the high-glucose condition, the activation of TGF-beta1/TAK1-induced phosphorylation and ubiquitination of SnoN protein resulted in reduced SnoN protein level as a consequence of enhanced SnoN degradation, which promoted EMT and ECM deposition in renal tubular epithelial cells.	Glucose	29-36	SKI like proto-oncogene	Homo sapiens	160-164
31028803-4	2019	KEY FINDINGS: Under the high-glucose condition, the activation of TGF-beta1/TAK1-induced phosphorylation and ubiquitination of SnoN protein resulted in reduced SnoN protein level as a consequence of enhanced SnoN degradation, which promoted EMT and ECM deposition in renal tubular epithelial cells.	Glucose	29-36	SKI like proto-oncogene	Homo sapiens	160-164
29709244-9	2018	Logistic regression indicated Snon-missense and Smissense-TP as predictors of ajmaline-induced PVCs.	Ajmaline	78-86	SKI like proto-oncogene	Homo sapiens	30-34
29970676-5	2018	Somehow, the expression of p-Smad3 and c-fos proteins significantly decreased in each of E2, bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) group, as well as the expression of SnoN protein significantly reduced only in BPA and NP groups, followed by TGF-beta3 treatment.	nonylphenol	125-127	SKI like proto-oncogene	Homo sapiens	187-191
29970676-5	2018	Somehow, the expression of p-Smad3 and c-fos proteins significantly decreased in each of E2, bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) group, as well as the expression of SnoN protein significantly reduced only in BPA and NP groups, followed by TGF-beta3 treatment.	octylphenol	134-145	SKI like proto-oncogene	Homo sapiens	187-191
29970676-5	2018	Somehow, the expression of p-Smad3 and c-fos proteins significantly decreased in each of E2, bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) group, as well as the expression of SnoN protein significantly reduced only in BPA and NP groups, followed by TGF-beta3 treatment.	bisphenol A	93-104	SKI like proto-oncogene	Homo sapiens	187-191
29970676-5	2018	Somehow, the expression of p-Smad3 and c-fos proteins significantly decreased in each of E2, bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) group, as well as the expression of SnoN protein significantly reduced only in BPA and NP groups, followed by TGF-beta3 treatment.	bisphenol A	106-109	SKI like proto-oncogene	Homo sapiens	187-191
29970676-5	2018	Somehow, the expression of p-Smad3 and c-fos proteins significantly decreased in each of E2, bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) group, as well as the expression of SnoN protein significantly reduced only in BPA and NP groups, followed by TGF-beta3 treatment.	nonylphenol	112-123	SKI like proto-oncogene	Homo sapiens	187-191
28350874-3	2017	High glucose stress induced significantly elevated SnoN, TGF-beta1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions.	Glucose	5-12	SKI like proto-oncogene	Homo sapiens	51-55
28765970-0	2017	BMP-7 enhances SnoN mRNA expression in renal tubular epithelial cells under high-glucose conditions.	Glucose	81-88	SKI like proto-oncogene	Homo sapiens	15-19
28707079-0	2018	Down-regulation of miR-23a inhibits high glucose-induced EMT and renal fibrogenesis by up-regulation of SnoN.	Glucose	41-48	SKI like proto-oncogene	Homo sapiens	104-108
28350874-3	2017	High glucose stress induced significantly elevated SnoN, TGF-beta1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions.	Glucose	5-12	SKI like proto-oncogene	Homo sapiens	126-130
28350874-4	2017	Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis.	Glucose	98-105	SKI like proto-oncogene	Homo sapiens	17-21
28350874-6	2017	Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy.	Glucose	78-85	SKI like proto-oncogene	Homo sapiens	15-19
26743567-0	2016	The downregulation of SnoN expression in human renal proximal tubule epithelial cells under high-glucose conditions is mediated by an increase in Smurf2 expression through TGF-beta1 signaling.	Glucose	97-104	SKI like proto-oncogene	Homo sapiens	22-26
26743567-11	2016	Taken together, the findings of this study demonstrate that the downregulation of SnoN expression in hRPTECs under high-glucose conditions is mediated by the increased expression of Smurf2 through the TGF-beta1/Smad signaling pathway.	Glucose	120-127	SKI like proto-oncogene	Homo sapiens	82-86
28115165-0	2017	Repression of Smad3 by Stat3 and c-Ski/SnoN induces gefitinib resistance in lung adenocarcinoma.	Gefitinib	52-61	SKI like proto-oncogene	Homo sapiens	39-43
28115165-4	2017	Here we show that signal transducer and activator of transcription (Stat)3 represses Smad3 in synergy with the potent negative regulators of TGF-beta signaling, c-Ski and SnoN, whereby renders gefitinib-sensitive HCC827 cells resistant.	Gefitinib	193-202	SKI like proto-oncogene	Homo sapiens	171-175
26743567-3	2016	In the present study, we demonstrated that the upregulation of Smad ubiquitination regulatory factor-2 (Smurf2), through TGF-beta1/Smad signaling, contributes to the downregulation of SnoN under high-glucose conditions in primary human renal proximal tubule epithelial cells (hRPTECs).	Glucose	200-207	SKI like proto-oncogene	Homo sapiens	184-188
26743567-7	2016	The protein levels of SnoN were markedly downregulated, while its mRNA levels were increased in the hRPTECs cultured under high-glucose conditions.	Glucose	128-135	SKI like proto-oncogene	Homo sapiens	22-26
26743567-9	2016	The knockdown of Smurf2 increased SnoN expression in the hRPTECs cultured in high-glucose medium.	Glucose	82-89	SKI like proto-oncogene	Homo sapiens	34-38
26743567-10	2016	Moreover, MG132 partially inhibited SnoN degradation in the hRPTECs under high-glucose conditions and SB-431542 decreased the phosphorylation of Smad2 and the expression of Smurf2 induced under high-glucose conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	SKI like proto-oncogene	Homo sapiens	36-40
23872350-0	2013	Downregulation of SnoN oncoprotein induced by antibiotics anisomycin and puromycin positively regulates transforming growth factor-beta signals.	Anisomycin	58-68	SKI like proto-oncogene	Homo sapiens	18-22
24637302-0	2014	PMA induces SnoN proteolysis and CD61 expression through an autocrine mechanism.	Tetradecanoylphorbol Acetate	0-3	SKI like proto-oncogene	Homo sapiens	12-16
23872350-0	2013	Downregulation of SnoN oncoprotein induced by antibiotics anisomycin and puromycin positively regulates transforming growth factor-beta signals.	Puromycin	73-82	SKI like proto-oncogene	Homo sapiens	18-22
23872350-3	2013	Intriguingly, the antibiotics anisomycin (ANS) and puromycin (PURO) are also able to downregulate Ski and SnoN proteins via proteasome.	Anisomycin	30-40	SKI like proto-oncogene	Homo sapiens	106-110
23872350-3	2013	Intriguingly, the antibiotics anisomycin (ANS) and puromycin (PURO) are also able to downregulate Ski and SnoN proteins via proteasome.	Anisomycin	42-45	SKI like proto-oncogene	Homo sapiens	106-110
23872350-3	2013	Intriguingly, the antibiotics anisomycin (ANS) and puromycin (PURO) are also able to downregulate Ski and SnoN proteins via proteasome.	Puromycin	51-60	SKI like proto-oncogene	Homo sapiens	106-110
23872350-3	2013	Intriguingly, the antibiotics anisomycin (ANS) and puromycin (PURO) are also able to downregulate Ski and SnoN proteins via proteasome.	Puromycin	62-66	SKI like proto-oncogene	Homo sapiens	106-110
23872350-6	2013	RESULTS: SnoN protein downregulation induced by ANS and PURO did not involve the induction of R-Smad phosphorylation but it was abrogated after TGF-beta signaling inhibition; this effect occurred in a cell type-specific manner and independently of protein synthesis inhibition or any other ribotoxic effect.	Anisomycin	48-51	SKI like proto-oncogene	Homo sapiens	9-13
23872350-6	2013	RESULTS: SnoN protein downregulation induced by ANS and PURO did not involve the induction of R-Smad phosphorylation but it was abrogated after TGF-beta signaling inhibition; this effect occurred in a cell type-specific manner and independently of protein synthesis inhibition or any other ribotoxic effect.	Puromycin	56-60	SKI like proto-oncogene	Homo sapiens	9-13
23621864-3	2013	We have previously shown that SnoN expression is increased in advanced stage ovarian cancers and alters cellular response to arsenic trioxide (As2O3).	Arsenic Trioxide	125-141	SKI like proto-oncogene	Homo sapiens	30-34
23621864-3	2013	We have previously shown that SnoN expression is increased in advanced stage ovarian cancers and alters cellular response to arsenic trioxide (As2O3).	Arsenic Trioxide	143-148	SKI like proto-oncogene	Homo sapiens	30-34
20508647-0	2010	Arsenic trioxide induces a beclin-1-independent autophagic pathway via modulation of SnoN/SkiL expression in ovarian carcinoma cells.	Arsenic Trioxide	0-16	SKI like proto-oncogene	Homo sapiens	85-89
23178716-7	2013	Collectively, As2O3 mediates an initial rise in pY-Src(416) to regulate the PI3K/AKT pathway which increases SnoN and cell survival; these early events may counter the cell death response associated with increased pY-EGFR/MAPK activation.	Arsenic Trioxide	14-19	SKI like proto-oncogene	Homo sapiens	109-113
23178716-0	2013	SnoN/SkiL expression is modulated via arsenic trioxide-induced activation of the PI3K/AKT pathway in ovarian cancer cells.	Arsenic Trioxide	38-54	SKI like proto-oncogene	Homo sapiens	0-4
23178716-0	2013	SnoN/SkiL expression is modulated via arsenic trioxide-induced activation of the PI3K/AKT pathway in ovarian cancer cells.	Arsenic Trioxide	38-54	SKI like proto-oncogene	Homo sapiens	5-9
23178716-2	2013	Arsenic trioxide (As2O3, used in treating APL) induces SnoN to oppose the apoptotic response in ovarian cancer cells.	Arsenic Trioxide	0-16	SKI like proto-oncogene	Homo sapiens	55-59
23178716-2	2013	Arsenic trioxide (As2O3, used in treating APL) induces SnoN to oppose the apoptotic response in ovarian cancer cells.	Arsenic Trioxide	18-23	SKI like proto-oncogene	Homo sapiens	55-59
20508647-0	2010	Arsenic trioxide induces a beclin-1-independent autophagic pathway via modulation of SnoN/SkiL expression in ovarian carcinoma cells.	Arsenic Trioxide	0-16	SKI like proto-oncogene	Homo sapiens	90-94
20508647-9	2010	The addition of N-acetyl-L-cysteine (ROS scavenger) to As(2)O(3)-treated cells reversed changes in SnoN protein and the autophagic/apoptotic response.	Acetylcysteine	16-35	SKI like proto-oncogene	Homo sapiens	99-103
20508647-9	2010	The addition of N-acetyl-L-cysteine (ROS scavenger) to As(2)O(3)-treated cells reversed changes in SnoN protein and the autophagic/apoptotic response.	ros	37-40	SKI like proto-oncogene	Homo sapiens	99-103
20508647-9	2010	The addition of N-acetyl-L-cysteine (ROS scavenger) to As(2)O(3)-treated cells reversed changes in SnoN protein and the autophagic/apoptotic response.	(2)o(3)	57-64	SKI like proto-oncogene	Homo sapiens	99-103
20508647-12	2010	Collectively, these findings suggest that As(2)O(3) induces a beclin-1-independent autophagic pathway in ovarian carcinoma cells and implicates SnoN in promoting As(2)O(3)-mediated autophagic cell survival.	(2)o(3)	164-171	SKI like proto-oncogene	Homo sapiens	144-148
20699661-0	2010	SnoN/SkiL, a TGFbeta signaling mediator: a participant in autophagy induced by arsenic trioxide.	Arsenic Trioxide	79-95	SKI like proto-oncogene	Homo sapiens	0-4
20699661-0	2010	SnoN/SkiL, a TGFbeta signaling mediator: a participant in autophagy induced by arsenic trioxide.	Arsenic Trioxide	79-95	SKI like proto-oncogene	Homo sapiens	5-9
20699661-6	2010	Based on our findings, we propose that As(2)O(3) induces a Beclin 1-independent autophagic pathway in ovarian carcinoma cells by modulating SnoN/SkiL expression, implicating SnoN as a novel therapeutic target for ovarian cancers.	(2)o(3)	41-48	SKI like proto-oncogene	Homo sapiens	140-144
20699661-6	2010	Based on our findings, we propose that As(2)O(3) induces a Beclin 1-independent autophagic pathway in ovarian carcinoma cells by modulating SnoN/SkiL expression, implicating SnoN as a novel therapeutic target for ovarian cancers.	(2)o(3)	41-48	SKI like proto-oncogene	Homo sapiens	145-149
20699661-6	2010	Based on our findings, we propose that As(2)O(3) induces a Beclin 1-independent autophagic pathway in ovarian carcinoma cells by modulating SnoN/SkiL expression, implicating SnoN as a novel therapeutic target for ovarian cancers.	(2)o(3)	41-48	SKI like proto-oncogene	Homo sapiens	174-178
17625116-4	2007	Treatment of HKC-8 cells with actinomycin D completely abolished HGF-mediated SnoN induction, suggesting its dependence on gene transcription.	Dactinomycin	30-43	SKI like proto-oncogene	Homo sapiens	78-82
19383336-3	2008	In both immortalized normal (TIOSE) and ovarian carcinoma cell lines (OVCA), SnoN RNA levels were increased by TGFbeta stimulation and altered by LY294002 and JNK II inhibitor treatment suggesting that the PI3K and JNK signaling pathways may regulate TGFbeta-induced increases in SnoN RNA.	tiose	29-34	SKI like proto-oncogene	Homo sapiens	77-81
20093492-9	2010	Furthermore, BMP-7 had no effect on Smad3 signaling after siRNA-mediated SnoN knockdown, whereas prevention of SnoN degradation with the proteasome inhibitor MG132 reproduced the inhibitory action of BMP-7 on Smad3 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	SKI like proto-oncogene	Homo sapiens	111-115
19383336-3	2008	In both immortalized normal (TIOSE) and ovarian carcinoma cell lines (OVCA), SnoN RNA levels were increased by TGFbeta stimulation and altered by LY294002 and JNK II inhibitor treatment suggesting that the PI3K and JNK signaling pathways may regulate TGFbeta-induced increases in SnoN RNA.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	146-154	SKI like proto-oncogene	Homo sapiens	77-81
19383336-5	2008	In contrast, in OVCA, SnoN levels were elevated 3h post-stimulation potentially as a result of inhibition of the proteosome.	Tritium	48-50	SKI like proto-oncogene	Homo sapiens	22-26
19383336-7	2008	In both TIOSE and OVCA, SnoN siRNA decreased cell growth between 20 and 50% concurrent with increased p21 levels.	tiose	8-13	SKI like proto-oncogene	Homo sapiens	24-28
19383336-7	2008	In both TIOSE and OVCA, SnoN siRNA decreased cell growth between 20 and 50% concurrent with increased p21 levels.	ovca	18-22	SKI like proto-oncogene	Homo sapiens	24-28
19383336-8	2008	In TIOSE, transient expression of SnoN repressed TGFbeta induction of PAI-1 promoters with little effect on the p21 promoter or resultant cell growth.	tiose	3-8	SKI like proto-oncogene	Homo sapiens	34-38
19383336-9	2008	In contrast to the effects of transient expression, stable expression of SnoN in TIOSE led to growth arrest through induction of senescence.	tiose	81-86	SKI like proto-oncogene	Homo sapiens	73-77
17625116-7	2007	In the promoter region of human SnoN gene, two cAMP response elements were located in close proximity to Sp1 sites.	Cyclic AMP	47-51	SKI like proto-oncogene	Homo sapiens	32-36
15967445-0	2005	Downregulation of Ski and SnoN co-repressors by anisomycin.	Anisomycin	48-58	SKI like proto-oncogene	Homo sapiens	26-30
16966324-7	2006	We identify lysine residues 50 and 383 as the SUMO acceptor sites in SnoN.	Lysine	12-18	SKI like proto-oncogene	Homo sapiens	69-73
17193924-5	2006	Furthermore, upregulation of three candidate genes (NFIL3, SKIL, and JMJD3) was shown to be dosage and time dependent with TPA treatment and was found to be directly regulated by TPA through PKC-dependent signaling.	Tetradecanoylphorbol Acetate	123-126	SKI like proto-oncogene	Homo sapiens	59-63
17193924-5	2006	Furthermore, upregulation of three candidate genes (NFIL3, SKIL, and JMJD3) was shown to be dosage and time dependent with TPA treatment and was found to be directly regulated by TPA through PKC-dependent signaling.	Tetradecanoylphorbol Acetate	179-182	SKI like proto-oncogene	Homo sapiens	59-63
15967445-2	2005	We have found that anisomycin is able to downregulate Ski and SnoN via proteasome as TGF-beta does, but through a mechanism independent of Smad activation.	Anisomycin	19-29	SKI like proto-oncogene	Homo sapiens	62-66
15967445-3	2005	The mechanism used by anisomycin to downregulate Ski and SnoN is also independent of MAPK activation and protein synthesis inhibition.	Anisomycin	22-32	SKI like proto-oncogene	Homo sapiens	57-61
15967445-4	2005	TGF-beta signal was the only pathway described causing Ski and SnoN degradation, thus this new effect of anisomycin on endogenous Ski and SnoN proteins suggests alternative processes to downregulate these negative modulators of TGF-beta signaling.	Anisomycin	105-115	SKI like proto-oncogene	Homo sapiens	63-67
15967445-4	2005	TGF-beta signal was the only pathway described causing Ski and SnoN degradation, thus this new effect of anisomycin on endogenous Ski and SnoN proteins suggests alternative processes to downregulate these negative modulators of TGF-beta signaling.	Anisomycin	105-115	SKI like proto-oncogene	Homo sapiens	138-142
34740826-7	2021	Our results indicate that lysine 343 localized in the SAND domain of SKIL constitutes a target for RNF111 ubiquitylation and demonstrate that RNF111 E3 ubiquitin ligase function specifically targets SKI and SKIL ubiquitylation and degradation upon TGF-beta pathway activation.	Lysine	26-32	SKI like proto-oncogene	Homo sapiens	69-73
11691834-6	2001	In addition to the D box, efficient ubiquitination and degradation of SnoN also requires the Smad3 binding site in SnoN as well as key lysine residues necessary for ubiquitin attachment.	Lysine	135-141	SKI like proto-oncogene	Homo sapiens	70-74
11691834-7	2001	Mutation of either the Smad3 binding site or lysine residues results in stabilization of SnoN and in enhanced antagonism of TGF-beta signaling.	Lysine	45-51	SKI like proto-oncogene	Homo sapiens	89-93
34605572-10	2021	Furthermore, rapamycin suppressed the increased expressions of MAD2B and SnoN induced by PDGF-BB.	Sirolimus	13-22	SKI like proto-oncogene	Homo sapiens	73-77
34605572-12	2021	Moreover, rapamycin exerts an inhibitory effect on intimal hyperplasia, possibly via the MAD2B-SnoN axis.	Sirolimus	10-19	SKI like proto-oncogene	Homo sapiens	95-99
34740826-7	2021	Our results indicate that lysine 343 localized in the SAND domain of SKIL constitutes a target for RNF111 ubiquitylation and demonstrate that RNF111 E3 ubiquitin ligase function specifically targets SKI and SKIL ubiquitylation and degradation upon TGF-beta pathway activation.	Lysine	26-32	SKI like proto-oncogene	Homo sapiens	207-211
2762147-6	1989	The first type, named snoN (non Alu-containing), encoded a protein of 684 amino acid residues.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	32-35	SKI like proto-oncogene	Homo sapiens	22-26
2762147-7	1989	The second type, named snoA (Alu-containing), encoded a protein of 415 amino acid residues.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	29-32	SKI like proto-oncogene	Homo sapiens	23-27