ABCMdb

ABCC8 p.Asn188Ser

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Publications

PMID: 16442101 [PubMed] Frelet A et al: "Insight in eukaryotic ABC transporter function by mutation analysis."

No. Sentence Comment

426 Shyng et al. [204] have reported that H125Q, N188S, F591L, T1139M, R1215Q and G1382S generated functional channels in the absence of ATP, indicating that the lack or reduction of KATP channel sensitivity to MgADP is a common molecular defect associated with the disease. Login to comment

PMID: 17466004 [PubMed] Muzyamba M et al: "Complex ABCC8 DNA variations in congenital hyperinsulinism: lessons from functional studies."

No. Sentence Comment

23 Whereas compound mutations occur in approximately 13% of CHI patients,39 the simultaneous presence of two homozygous CHI mutations has to our knowledge only been reported in one patient, in which one of the mutations (N188S) was thought to be nonfunctional.40 In this report,we describe two patients with more than one suspected mutation in diffuse and focal disease and delineate the consequences these DNA variations have on KATP channel function. Login to comment

PMID: 9648840 [PubMed] Shyng SL et al: "Functional analyses of novel mutations in the sulfonylurea receptor 1 associated with persistent hyperinsulinemic hypoglycemia of infancy."

No. Sentence Comment

2 We have studied the functional properties of novel SUR1 mutations identified in PHHI patients, including H125Q, N188S, F591L, T1139M, R1215Q, G1382S, and R1394H. Login to comment
3 R1394H and F1388 SUR1, a previously identified PHHI mutation, resulted in no functional channels when coexpressed with Kir6.2 in COS cells, while H125Q, N188S, F591L, T1139M, R1215Q, and G1382S SUR1 generated functional channels in the absence of ATP. Login to comment
4 With the exception of N188S and H125Q, all mutants had reduced response to stimulation by MgADP. Login to comment
75 The positions of the seven newly identified SUR1 mutations that are associated with the disease PHHI are shown in Fig. 1, including H125Q, N188S, F591L, T1139M, R1215Q, G1382S, and R1394H on both SUR1 topology models. Login to comment
112 Compared with wild-type channels, H125Q had a slightlygreater response to diazoxide (P < 0.1, ANOVA), N188S hada response that is similar to the wild-type channel (NS, ANOVA), T1139M and G1382S mutant channels had slightly reduced responses, while F591L and R1215Q channels had severely reduced responses (P < 0.005 and 0.025, respectively, ANOVA) (Fig. 6). Login to comment
138 One patient was homozygous for the N188S mutation and another compound heterozygousforthis mutation and a novel splice-site mutation 3992-3 c-to-g (M.A.P., B.G., unpublished observations). Login to comment
156 With the exception of N188S and H125Q, which formed channels that were indistinguishable from the wild-type in terms of regulation of the channel by nucleotides and diazoxide, all other mutants caused defects of various severity in the resulting channels. Login to comment
163 This is particularly true of the N188S mutation, which alters channel function only minimally in vitro but is associated with severe clinical disease. Login to comment
175 Five others (H125Q, N188S, F591L, T1139M, and R1215Q) are outside of the predicted nucleotide-binding folds. Login to comment
176 However, except for N188S and H125Q, these mutations all show some defects in regulation of the channel by MgADP or by diazoxide. Login to comment
183 1150 DIABETES, VOL. 47, JULY 1998 SUR1 MUTATIONS AND KATP CHANNELS TABLE 1 Clinical characteristics of the PHHI patients bearing SUR1 mutations Clinical Diazoxide Patient Allele 1 Allele 2 Onset severity responsiveness Treatment G2,4 F1388 F1388 <1 week Severe No Octreotide H2 N188S N188S ?? Login to comment
185 Pancreatectomy BV N188S 3992-3 c-to-g <1 week Severe No Pancreatectomy CB H125Q F1388 1 year Mild No Pancreatectomy Q R1215Q 3992-9 g-to-a <1 week Severe Inadequate Pancreatectomy AO R1394H 3992-9 g-to-a < week Severe No Pancreatectomy BI F591L - <1 week Mild Yes Diazoxide BU G1382S - <1 week Severe ?? Login to comment

PMID: 9618169 [PubMed] Nestorowicz A et al: "Genetic heterogeneity in familial hyperinsulinism."

No. Sentence Comment

63 Mutations within the SUR1 gene Patient Exon or intron Nucleotide changea Codona predicted effect Domainb Restriction site change Frequency (%) HI chromosomes (n = 88) Segregation demonstrated Frequency 200 normal chromosomes A1 exon 2 221G→A R74Q Tm PstI 1 (1.1%) NA 0 B2d exon3 375C→G H125Q Tm DdeIc 1 (1.1%) NA 0 C3e exon 4 563A→G N188S Tm TspRI 1 (1.1%) yes 0 D4 exon 6 949delC 317fs/ter Tm Bsp1286I 1 (1.1%) yes 0 E5 exon 8 1216A→G N406D Tm XcmI 1 (1.1%) NA 0 F6f intron 10 1630+1G→T aberrant splicing Tm BsrI 2 (2.3%) yes 0 G7 exon 12 1773C→G F591L Tm BsoF1 1 (1.1%) no 0 H8 exon 13 1893delT 631fs/ter Tm BstNI 1 (1.1%) yes 0 F6f intron 15 2117-1G→A aberrant splicing NBF-1 PstI 1 (1.1%) yes 0 I9 exon 24 2860C→T Q954X - BstNI 1 (1.1%) yes 0 J10g exon 28 3416C→Th T1139M Tm NlaIII 1 (1.1%) yes 0 K11 exon 29 3644G→A R1215Q Tm NciI 1 (1.1%) yes 0 J10g intron 32 3992-9G→Ai aberrant splicing NBF-2 NciI 4 (4.5%) yes 0 C3e intron 32 3992-3C→G aberrant splicing NBF-2 AvaI 1 (1.1%) yes 0 L12 exon 34 4135G→C G1379R NBF-2 EagI 1 (1.1%) yes 0 M13 exon 34 4144G→A G1382S NBF-2 BglI 1 (1.1%) yes 0 B2d exon 34 4162delTTCi,j delF 1388 NBF-2 BseRI 1 (1.1%) yes 0 J10g exon 34 4181G→Ah R1394H NBF-2 DraIII 1 (1.1%) yes 0 N14 exon 35 4310G→Ai aberrant splicing NBF-2 MspI 1 (1.1%) yes 0 O15 exon 37 4525insCGGCTT insertion of AlaSer ft d 1508 NBF-2 PvuIIk 1 (1.1%) yes 0 after codon 1508 aNucleotide and codon positions are according to the full-length human SUR1 cDNA sequence incorporating the alternative splicedform of exon 17 (GenBank accession nos L78208 and L78216). Login to comment
200 A model for SUR1 (29) predicts that the remaining seven missense mutations (Arg74Gln, His125Gln, Asn188Ser, Asn406Asp, Phe591Leu, Thr1139Met, Arg1215Gln) are located either within transmembrane segments or are present on the extracellular or cytoplasmic loops connecting adjacent trans- membranehelices.Theidentificationofthesemissensemutations in HI patients provides a basis for further studies to elucidate the functions of these transmembrane domains in SUR1 and KATP channel activity. Login to comment

PMID: 11697420 [PubMed] Christesen HB et al: "Pancreatic beta-cell stimulation tests in transient and persistent congenital hyperinsulinism."

No. Sentence Comment

12 Compound heterozygosity for the SUR1 mutations 3992-3c to g and N188S was found. Login to comment
111 The maternal exon 5 missense mutation N188S has also been found in a homozygous proband with severe HI (12). Login to comment

PMID: 15562009 [PubMed] Henwood MJ et al: "Genotype-phenotype correlations in children with congenital hyperinsulinism due to recessive mutations of the adenosine triphosphate-sensitive potassium channel genes."

No. Sentence Comment

54 Gene Haplotype Calcium (␮U/ml) Leucine (␮U/ml) Glucose (␮U/ml) Tolbutamide (␮U/ml) Diazoxide responsive Diffuse HI 1 SUR1 delF1388/D1472H 6 2 13 -2 No 2 Kir6.2 G134A/P266L 20 3 36 -2 No 3 SUR1 g3992-9a/g1630ϩ1a 11 16 -2 No 4 SUR1 N188S/D1472N 7 1 7 7 No 5 SUR1 R598X/R999X 32 1 72 27 No 6 SUR1 R495Q/R1215Q -2 15 44 30 No 7 SUR1 R74W/R1215Q 52 28 20 98 No 8 SUR1 g3992-9a/K1337N 2 18 39 33 Yes Focal HI 9 SUR1 F27S 17 -1 16 29 No 10 SUR1 F686S 12 2 27 12 No 11 SUR1 E501K 6 3 9 10 No 12 SUR1 3576delg 9 6 9 12 No 13 SUR1 g3992-9a 5 8 25 9 No 14 SUR1 g3992-9a 3 8 40 21 No 15 SUR1 c2924-10a 4 8 67 29 No 16 Kir6.2 A101D 1 8 177 88 No 17 SUR1 R1215W 7 9 15 6 No 18 Kir6.2 R136L 8 10 115 21 No 19 SUR1 g3992-9a 40 15 35 -0.3 No 20 SUR1 6aa insertion in exon 5 6 16 22 15 No 21 SUR1 R1215W 38 47 58 15 No 22 Kir6.2 R301H 16 55 75 14 No Controls (␮U/ml, mean Ϯ SD) KATP HI (n ϭ 7) 28 Ϯ 16 5 Ϯ 8 12 Ϯ 9 4 Ϯ 6 No GDH-HI (n ϭ 7) 2.3 Ϯ 5.4 42 Ϯ 27 120 Ϯ 52 94 Ϯ 56 Yes Normal (n ϭ 6) 3 Ϯ 4 1.4 Ϯ 2.8 56 Ϯ 26 48 Ϯ 32 Yes a To convert insulin (␮U/ml to pmol/liter), multiply by 6.0. identified in other patients. Login to comment
107 Degree of residual channel function in KATP mutations Null Indeterminate Partial SUR1 g3992-9a g1630ϩ1a R598X/R999X delF1388 N188S/D1472N R495Q/R1215Q F27S 3576delg R74W/R1215Q F686S K1337N E501K 6 aa insertion in exon 5 c2924-10a R1215W Kir6.2 G134A/P266L R301H A101D R136L FIG. 1. Login to comment

PMID: 16429405 [PubMed] Fernandez-Marmiesse A et al: "Mutation spectra of ABCC8 gene in Spanish patients with Hyperinsulinism of Infancy (HI)."

No. Sentence Comment

106 Mutations c.220C>T (p.R74W), c.331G>C (p.G111R), and c.563A>G (p.N188S) are situated in the TMD0 domain of SUR1 which is implicated in the strong association between SUR1 and Kir6.2 and modulate trafficking and gating of the channel (Chan et al. 2003). Login to comment
109 Finally, mutation N188S detected in homozygosis in patient P25 had been previously reported by Nestorowicz et al. (1998) associated with severe clinical disease, although it was reported by Shyng et al. (1998), that this mutation alters channel function only minimally in vitro. Login to comment
111 This substitution appears as a pathogenic mutation in the Human Gene Mutation Database which seems to support that N188S produces a non pathogenic change. Login to comment
137 Clinical characteristics of HI Spanish patients that carry at least one mutation in ABCC8 Mutationsg Pa Ob Sex Mc Td PCe PTf Pchrh Mchrh 1a Gal M >p90 DZ 5 (>90%) OT, NF, GC p.R248X c.3576delG 1b Gal F >p50 DZ, OT, NF - OT, NF, NGT p.R248X c.3576delG 3 Gal F >p90 DZ 2 (95%) - c.584 585insA c.584 585insA 4 Gal M >p75 DZ 4 (95%) DZ, NGT c.584 585insA c.584 585insA 5 Gal M >p50 OT, DZ 16 (90%) - c.1347 1348delGA - 8 Cast M >p75 DZ, OT, GC - - p.M233R - 9 Cast F >p75 DZ 0.5 (85%) DZ, OT, PC (99%) p.G111R - 12 And M - - - - c.4612 -2 A>T p.D310N 14 Cat M >p75 DZ - - p.R934X c.3992-9 G>A 17 Cat F >p90 DZ, OT - - c.3133 3152del c.4619 4620insT 18 Cat M <p50 DZ, CNF 0.5 (95%) DZ c.1732 1746dup - 19 Can M <p50 DZ, NF, OT 2 (99%) - c.1332+4438 1631-9207del c.1332+4438 1631-9207del 20 Cat M - DZ, NF, GC - - c.2142delG p.T1131P 21 Cat F >p50 DZ, NF - - - i - i 23 Bal M >p90 CNF - - c.4310 G>A c.1732 1746dup 25 Mor M - DZ, OT yes (EXITUS) p.N188S, c.4123-19 C>T p.N188S, c.4123-19 C>T 27 Cast F >p75 DZ, CNF 24 (75%) PC (99%) p.R598X p.L1451P 28 Cat M >p90 DZ, CNF - - p.R1251X p.L1148R 30 Cast M >p90 DZ, OT 5 (95%) DZ, OT (EXITUS) p.R74W - 31 Gal F >p90 DZ 0.5 (95%) DZ - p.K719T 32 Cat F >p90 DZ - - - p.N1296K 33 Cast F >p75 DZ, OT 1 (95%) DZ, OT c.3291 3292delGC - 34 Val F >p90 DZ, NF - (EXITUS) p.P551R - a P = patient. Login to comment
147 Genetic variants found in ABCC8 gene from HI Spanish cohort Mutations considered pathogenic nt change a aa change a Type E/Ic Domaind Patient Refe PSIC f Polypheng C h c.220C>T p.R74W MIS E2 CL1 P30 NR 2.257 PrD Highly c.331G>C p.G111R MIS E3 TM3 P9 [1] 1.672 PsD Moderately c.563A>G p.N188S MIS E4 TM5 P25 [2] 1.494 Benign Highly c.698T>G p.M233R MIS E5 CL3 P8 NR 2.428 PrD Highly c.584_585insA p.Y195X FS E5 ─ P3, P4 NR ─ ─ ─ c.742C>T p.R248X NON E5 ─ P1a, P1b [3] ─ ─ ─ c.928G>A p.D310N MIS E6 CL3 P12 NR 1.614 PsD Highly c.1347_1348delGA p.V449VfsX493 FS E9 ─ P5 NR ─ ─ ─ c.1332+4438_1631-9207del p.I445FfsX447 FS ─ ─ P19 NR ─ ─ ─ c.1652C>G p.P551R MIS E11 TM10 P34 NR 2.1 PsD Highly c.1732_1746dup p.A578_L582dup IFins E12 ─ P18, P23 NR ─ ─ ─ c.1792C>T p.R598X NON E12 ─ P27 NR ─ ─ ─ c.2156 A>C p.K719T MIS E16 CL6 P31 NR 1.927 PsD Highly c.2142delG p.Q714QfsX724 FS E16 ─ P20 NR ─ ─ ─ c.2394-2A>G ─ AS I19 ─ P21 NR ─ ─ ─ c.2800C>T p.R934X NON E23 ─ P14 NR ─ ─ ─ c.3133_3152del p.L1045LfsX1107 FS E25 ─ P17 [6] ─ ─ ─ c.3291_3292delGC p.L1097LfsX1113 FS E26 ─ P33 NR c.3391A>C p.T1131P MIS E27 CL7 P20 NR 1.777 PsD Moderately c.3443T>G p.L1148R MIS E28 TM14 P28 NR 1.722 PsD Highly c.3576delG p.L1191LfsX1207 FS E29 ─ P1a, P1b, NR ─ ─ ─ c.3751C>T p.R1251X NON E30 ─ P28 NR ─ ─ ─ c.3888C>G p.N1296K MIS E32 TM17 P32 NR 1.924 PsD Highly c.3992-9G>A ─ AS I 32 ─ P14 [4] ─ ─ ─ c.4123-19C>T ─ AS I33 ─ P25 [5] ─ ─ ─ c.4310G>A ─ AS E35 ─ P23 [4] ─ ─ ─ c.4352T>C p.L1451P MIS E36 CL9 P27 NR 1.797 PsD Highly c.4612-2 A>T ─ AS I38 ─ P12 NR ─ ─ ─ c.4619_4620insT p.H1540AfsX1559 FS E39 ─ P17 NR ─ ─ ─ Polimorphisms and unclassified variants nt change a aa change a Type E/Ic SNPid Patientsi Controls NCBI j Exclusion c. 207T>C p.P69P SYN E2 rs1048099 28/46 ─ 0.50 S c. 330C>T p.A110A SYN E3 rs8192695 2/48 ─ 0.04 S c. Login to comment
166 ESEfinder score change of some variants of ABCC8 gene nt change aa change ESE changes a SF2-ASF SC35 SRp40 SRp55 Mutations c.220C>T R74W Lost 2.9 Gain 0.64 Gain 1.49 Lost 1.55 c.331G>C G111R M 2.58 - - - c.563A>G N188S - M 0.36 - Gain 0.61 c.2156 A>C K719T - - - Gain 2.14 c.3391A>C T1131P Lost 1.74 c.3443T>G L1148R M +2.12 Gain 2.39 c.3888C>G N1296K ─ ─ Lost 1.73 ─ c.4352T>C L1451P M -0.42 Lost 0.65 Gain 1.54 ─ Polymorphisms and unclassified variants c. 207T>C P69P Gain 1.458 M -0.645 ─ ─ c. 330C>T A110A M -2.524 ─ ─ ─ c. 1686C>T H562H ─ Lost-0.645 M -0.356 M +1.551 c. 1707C>T* A569A Lost 2.397 ─ ─ ─ c. 1947G>A K649K ─ ─ Lost 0.846 M -0.609 c. 2280C>T T760T Lost 2.524 ─ M +0.356 ─ c. 3822G>A R1274R M -2.824 Lost 2.382 ─ c. 4108T>G S1370A ─ M +0.648 ─ ─ c. 4717G>A V1573I ─ ─ M -0.609 a Lost (or gain) of an ESE below (above) the threshold values (SF2-ASF = 1.956; SC35 = 2.383; SRp40 = 2.67; SRp55 =2.676; Cartegni et al. 2003) are indicated. Login to comment

PMID: 14715863 [PubMed] Stanley CA et al: "Preoperative evaluation of infants with focal or diffuse congenital hyperinsulinism by intravenous acute insulin response tests and selective pancreatic arterial calcium stimulation."

No. Sentence Comment

205 of alleles SUR1 region Exon 1 F27Sa 1 Exon 2 R74W 2 Exon 4 536-9 del atgga 1 Exon 4 N188S 1 Exon 5 ins 6a.a. 1 Exon 10 R495Qa 1 Exon 10 E501Ka 1 Intron 10 g 1630ϩ1 aa,b 1 Exon 12 R598X 1 Exon 13 1874 del c 1 Exon 15 F686Sa 1 Exon 16 C717X 1 Intron 24 c 2924-9 aa 1 Exon 24 2835-8 del agaga 2 Exon 24 Q954X 1 Exon 25 R999X 2 Exon 29 3576 del g 1 Exon 29 R1215Q 2 Exon 29 R1215Wa,b 2 Intron 32 g 3992-9 a 4 Exon 33 L1350Qa 1 Exon 33 G1401Ra 1 Exon 34 S1387F 1 Exon 34 delF1388 1 Exon 36 D1472Ha 1 Exon 36 D1472Na 1 Kir6.2 region A102Na 1 G134A 1 R136La 1 P266L 1 R301Ha 1 a Novel mutations. Login to comment

PMID: 10334322 [PubMed] Otonkoski T et al: "A point mutation inactivating the sulfonylurea receptor causes the severe form of persistent hyperinsulinemic hypoglycemia of infancy in Finland."

No. Sentence Comment

212 Interestingly, one of these mutations (N188S) lies adjacent to that reported here, at the cytosolic end of the predicted fifth transmembrane domain (using the topology of Tsnuandy et al. [28]). Login to comment
213 The N188S mutation does not alter the sensitivity of the KATP channel to ATP or Mg-ADP, butappears to reduce the level of functional expression (31). Login to comment
214 The V187D mutation appears to be more severe than N188S, as we could not observe any KATP channel activity in excised patches. Login to comment

PMID: 11723059 [PubMed] Kassem SA et al: "p57(KIP2) expression in normal islet cells and in hyperinsulinism of infancy."

No. Sentence Comment

82 Sex Birth weight (kg) Age of onset (months) Age at surgery (months) Postoperative status Paternal mutation Maternal mutation Diffuse HI 1 F 4.1 1.25 1.5 Hypoglycemic 3992-3 c to g N188S 2 M 3.6 Birth 1.6 Diabetes delcP317 delcP317 3 M 5.04 Birth 3.25 Hypoglycemic Kir Y12X Kir Y12X 4 M 4.4 Birth 13 Hypoglycemic 3992-9 g to a delF1388 Focal HI 5 M 5.36 Birth 0.5 Euglycemic 3992-9 g to a None found 6 M 3.19 Birth 2 Euglycemic R1494Q None found 7 F 3.3 5 6 Euglycemic No DNA - 8 F 3.25 Birth 0.833 Euglycemic None found* None found 9 M 4.18 Birth 1.25 Diabetes None found None found 10 M 3.61 Birth 5.5 Euglycemic None found None found 11 F 3 Birth 12 - No DNA - 12 M 4 Birth 1.5 Diabetes None found None found 13 M 3.9 Birth 2 Euglycemic No DNA - 14 M 3.8 Birth 3 Diabetes No DNA - 15 M 3.63 10 11 Euglycemic A1493T None found Subjects 1-13 were evaluated for p57K1P2 expression, whereas subjects 8-15 were evaluated for IGF-II expression. Login to comment

PMID: 24686051 [PubMed] Demirbilek H et al: "Clinical characteristics and phenotype-genotype analysis in Turkish patients with congenital hyperinsulinism; predominance of recessive KATP channel mutations."

No. Sentence Comment

67 The remaining six ABCC8 mutations, p.R168C, p.N188S, p.L533P, p.W232G, p.R842Q and p.F591L were each identified in a single patient. Login to comment
85 Gene Current age (year) Exon/intron DNA description Protein description Consequence Transmission Treatment Follow-up Developmental delay Comments Diazoxide responsive Octreotide responsive Pancreatectomy (histology) ABCC8 1 3.9 Exon 28 c.3554COA p.Ala1185Glu Missense Homozygous K C K Octreotide CCC Novel mutation 2 0.7 Exon 28 c.3554COA p.Ala1185Glu Missense Homozygous K C K Octreotide Novel mutation 3 9.1 Exon 28 c.3554COA p.Ala1185Glu Missense Homozygous K K K Irregular CCCC Novel mutation 4 0.7 Exon 28 c.3554COA p.Ala1185Glu Missense Homozygous K C K Octreotide C Novel mutation 5 0.2 Exon 28 c.3554COA p.Ala1185Glu Missense Homozygous K C K Octreotide Novel mutation 6 0.7 Exon 28 c.3512delT p.Leu1171fs Frameshift Homozygous K K C (diffuse) Remission 7 0.7 Exon 28 c.3512delT p.Leu1171fs Frameshift Homozygous K C C (diffuse) Octreotide 8 Died Exon 28 c.3512del p.Leu1171fs Frameshift Heterozygous paternal K K C (diffuse) Died 9 5.8 Exon 28 c.3512delT p.Leu1171fs Frameshift Homozygous K C K Octreotide CCC Ectodermal dysplasia 10 9.6 Exon 28 c.3512delT p.Leu1171fs Frameshift Homozygous K C K Octreotide CCC 11 0.7 Exon 4 c.502COT c.563AOG p.Arg168Cys/ p.Asn188Ser Missense Compound heterozygous K C C (diffuse) Octreotide K 12 Died Exon 10 c.1598TOC p.Leu533Pro Missense Homozygous K C K Died Novel mutation 13 10.6 Exon 5/ exon 21 c.694TOG/ c.2525GOA p.Trp232Gly/ p.Arg842Gln Missense/ Missense Compound heterozygous K C K Octreotide CC 14 5.5 Exon 12 c.1771TOC p.Phe591Leu Missense Heterozygous C K Diazoxide K KCNJ11 15 2.4 Exon 1 c.101GOA/ c.376GOA p.Arg34His/ p.Glu126Lys Missense/ Missense Compound heterozygous K C K Octreotide K 16 3.3 Exon 1 c.272GOA p.Trp91X Nonsense Homozygous K C C (diffuse) Octreotide CC 17 3.2 Exon 1 c.376GOA p.Glu126Lys Missense Homozygous K C C (diffuse) Octreotide CC HADH 18 4.4 Exon 6 c.706COT p.Arg236X Nonsense Homozygous C Diazoxide C Genotype-phenotype correlation " Comparison between KATP mutation-positive and KATP mutation-negative groups highlighted a statistically significant increased birth weight and younger age of presentation in KATP mutation-positive group as compared with KATP mutation-negative patients (Table 3). Login to comment