Publication for ACLY and HMGCS1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	ACLY	ATP citrate lyase	47			[link]
hsa	HMGCS1	3-hydroxy-3-methylglutaryl-CoA synthase 1	3157

Pubmed ID	Priority	Text
31651237	0.98	ACLY, ACSS2, INSIG1, HMGCR, HMGCS1, and LPIN1 were also validated by RT-qPCR (Fig. 7).
	0.97	ACLY, HMGCS1, INSIG1, LPIN1, HMGCR, and ACSS2 were found to be significantly upregulated in comparison groups Mock vs. MBV6h, Mock vs. MBV 12 h, and Mock vs. MBV24h groups.
	0.95	ACLY, HMGCS1, INSIG1, LPIN1, HMGCR, and ACSS2 in group MBV2h vs. MBV6h (Additional file 7).
	0.95	ACLY, ACSS2, INSIG1, HMGCR, HMGCS1, LPIN1, validated by RT-qPCR.
	0.85	ACLY, HMGCS1, FDFT1, were the three genes with the most node degree in the analysis, labelled in red blot, green blot and yellow blot, respectively
29226804	0.98	ACLY, ACAT2, HMGCS1, MVD, IDI1, and FPDS) (Figure 3B).
	0.97	ACLY and ACSS2 (Figure 3A) were, except for HMGCS1 knockdown, as predicted by the core regulation model (Figures 3B and 3E).
	0.97	ACLY, HMGCS1, IDI1, LSS, NSDHL, and FDFT1), confirming that this is the main affected cellular pathway.
21561152	0.98	ATP citrate lyase, ACL; insulin induced gene 1, INSIG1; mevalonate pyrophosphate decarboxylase, MVD; HMGCoA synthase 1, HMGCS; isopentenyl-diphosphate delta isomerase 1, IDI1; stearoyl-CoA desaturase, SCD1; LDL receptor, LDLR; ribosomal protein L13a, RPL13A; beta- 2 microglobulin, B2M; glyceraldehyde-3-phosphate dehydrogenase, GAPDH.
24493696	0.97	ACL, FASN, SCD-1, HMGCS1, HMGCR, MVK, MVD and LDLR and two chaperones, INSIG-1 and SCAP in LNCaP and C4-2B cells examined by qRT-PCR.
	0.97	ACL, FASN, SCD-1, HMGCS1, HMGCR, MVK and MVD and two chaperones, INSIG-1 and SCAP compared to the control group.
	0.96	ACL, FASN and SCD-1 for lipogenesis, HMGCS1, HMGCR, MVK, MVD and LDLR for cholesterogenesis, two chaperones, INSIG1 and SCAP.
	0.54	ACL, FASN, SCD-1, HMGCS1, HMGCR, MVK, MVD, INSIG1 and SCAP (Fig. 5A).
31932581	0.97	ACLY, ACC1, FASN, SCD1) and cholesterol synthesis (HMGCS1, HMGCR).
	0.97	ACLY, ACC1, SCD1 and HMGCS1 were observed when SIK2 was knockdown or overexpressed in A2780 and SKOV3 cells.
	0.81	ACLY, ACC1, FASN, SCD1, HMGCS1 and HMGCR in A2780 and SKOV3 cells with treatment as indicated.
26535009	0.97	HMGCS1, DHCR7, DHCR24, LDLR, FDFT1, FDPS, IDI1, MVD, SQLE, LSS, NSDHL, SC5DL, INSIG1, ACLY, and ACSS2 (see fig. S1 for full list).
	0.69	ACLY [ATP citrate lyase], and ACC [acetyl-CoA carboxylase]) whereas SREBP-2 predominantly activates genes involved in cholesterol metabolism (including HMGCR, HMGCS1, and LDLR) .
29153836	0.97	ACLY, ACSS2, HMGCS1, MVD, and FDFT1 (highlighted in red, Figure 4C).
	0.88	ACLY, ACSS2, HMGCS1, and MVD was markedly decreased by SRPK2 knockdown as well as by rapamycin treatment (Figure 5D).
22886728	0.97	ATP-citrate lyase (ACLY), hexokinase-2 (HK2), low-density lipoprotein receptor (LDLR), acyl-CoA synthetase short-chain family member 2 (ACSS2), and 3-hydroxy-3-methylglutaryl-coenzyme A synthase-1 (soluble) HMGCS1 and down-regulation of acyl-CoA synthetase short-chain family member-1 (ACSS1) in majority of the NSCLC cell lines studied (Fig. S3 in the "Electronic Supplementary Material").
29851839	0.97	ACLY participated in the TCA cycle; FDPS in terpenoid backbone biosynthesis and metabolism; ADH1A in oxidoreductase activity and alcohol dehydrogenase (NAD) activity; ACAT2 in metabolism and fatty acid metabolism; AKR1C1 in oxidoreductase activity and acting on NAD(P)H; and HMGCS1 in terpenoid backbone biosynthesis and metabolism.
26918450	0.96	ACL by phosphorylation and activate the expression of several genes involved in fatty acid and cholesterol biosynthesis, such as FASN, ACC, ACL, ACAT, HMGCS and HMGCR, through their effects on the transcription factor family of sterol regulatory element-binding proteins (SREBPs).
	0.65	ACL, ATP citrate lyase; ASAH1, N-acylsphingosine amidohydrolase (acid ceramidase) 1; DHCR24, 24-dehydrocholesterol reductase; ENO1, enolase 1, (alpha); FASN, fatty acid synthase; GPT, alanine aminotransferase; G6PD, glucose-6-phosphate dehydrogenase; HADHA, hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase (trifunctional protein), alpha subunit; HMGCR, HMG-CoA reductase; HMGCS, HMG-CoA synthase; IDH2, isocitrate dehydrogenase 2 (NADP+), mitochondrial; LDHA, lactate dehydrogenase A; LPL, lipoprotein lipase; MDH1, malate dehydrogenase 1, NAD (soluble); MDH2, malate dehydrogenase 2, NAD (mitochondrial); ME1, malic enzyme 1, NADP+-dependent, cytosolic; ME3, malic enzyme 3, NADP+-dependent, mitochondrial; MSMO1, methylsterol monooxygenase 1; PC, pyruvate carboxylase; PCCB, propionyl CoA carboxylase, beta polypeptide; PCK2, phophoenolpyruvate carboxykinase 2 (mitochondrial); PDH, pyruvate dehydrogenase complex; PGAM1, phosphoglycerate mutase 1 (brain); PGM1, phosphoglucomutase 1, PHGDH, phosphoglycerate dehydrogenase; PK, pyruvate kinase; PSAT1, phosphoserine aminotransferase 1; SPTLC3, serine palmitoyltransferase, long chain base subunit 3; TM7SF2, transmembrane 7 superfamily member 2.
22684502	0.96	Acly, Acat2, Aacs, Hmgcs1, Mvd, Idi1, Fdft1, Tm7sf2, Ebp, Nsdhl, Sc5d and Dhcr24) (Figure 7A).
24203995	0.94	ACLY, ATP citrate lyase; AGPAT, 1-acylglycerol-3-phosphate O-acyltransferase; COX1/2, prostaglandin-endoperoxide synthase (PTGS); DGAT, diacylglycerol O-acyltransferase; ELOVL, fatty acid elongase; FADS, fatty acid desaturase; FASN, fatty acid synthase; GPAT, glycerol-3-phosphate acyltransferase; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; HMGCS, 3-hydroxy-3-methylglutaryl-CoA synthase; PPAP, phosphatidic acid phosphatase; SCD, stearoyl-CoA desaturase; SPHK, sphingosine-1-kinase.
31316083	0.93	ACLY and HMGCS1 expression using normalized RNA-Seq data from the SKCM group in TCGA and the normal skin tissue group in GTEx.
20478529	0.89	HMGCS1, ACACA, and ACLY were actually higher in the adapted cells (Fig. 7E-I).
31159827	0.78	HMGCS1 gene), fatty acid synthesis (FASN, ACLY genes) and TCA (tricarboxylic acid) cycle (SDHA, FH genes).
32117236	0.75	ACLY, HMGCR, HMGCS1, CYP51A1, and LCLAT1), while cluster 2 genes showed enrichment for the terms epidermal development (GRHL3, KRT17, SPRR1A, and SPRR1B) and tumor antigen (MAGEA2, MAGEA3, MAGEA6, and MAGEA9B) (Figure 6B), suggesting possible roles for these biological processes in the promotion of the T cell-cold phenotype.
24280005	0.73	ACLY, HMGCR or HMGCS failed to cause CHOP induction suggesting that inhibition of fatty acid or cholesterol biosynthesis is not sufficient to induce ER-stress (Additional file 5: Figure S3C, D, E).
25153832	0.63	ACLY, FDPS, HMGCS1 and LSS were significantly upregulated.