Publication for Hmgcr and Insig1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357			[link]
mmu	Insig1	insulin induced gene 1	231070

Pubmed ID	Priority	Text
31323021	0.99	HMGCR with Insig-1 conferred sterol-regulated degradation of endogenous HMGCR, as Insig-1 is a rate-limiting co-factor for multiple E3s including gp78, TRC8 and RNF145 (Fig 1B, lanes 1-2).
	0.98	Insig-1 for HMGCR binding, thereby preventing HMGCR from degradation and increasing cholesterol biosynthesis.
	0.98	Insig-1 mediated HMGCR degradation.
	0.98	HMGCR binding to ER-anchored Insig-1 and Insig-2, which bring ubiquitin ligases gp78, TRC8 and RNF145 together with other cofactors to ubiquitinate HMGCR, resulting in its degradation in proteasome.
	0.98	HMGCR binding to Insig-1 or Insig-2, which recruits E3 ubiquitin ligases including gp78, TRC8 and RNF145 for ubiquitination and proteasomal degradation of HMGCR.
	0.98	Insig-1 for binding to HMGCR.
	0.97	Insig-1 for binding HMGCR, preventing the latter from ubiquitination and degradation.
21812109	0.98	Hmgcr by 6h likely via complex changes in SREBP, Insig1 and Insig2, indicating that acrolein action likely begins with transcriptional changes in sterol regulatory factors.
	0.98	Hmgcr and Insig1 transcription, yet both these genes are down-regulated by acrolein.
	0.97	Insig1, Insig2 and Hmgcr genes and stimulated an acute phase response (APR) with up-regulation of serum amyloid A genes (Saa) and systemic hypoalbuminemia.
	0.77	Hmgcr and Insig1 mRNAs, but it appears this is not HMGCR activity-dependent.
26311497	0.98	Insig-1 mediates HMGCR degradation via interaction with gp78 and VCP under cholesterol sufficient condition.
	0.97	HMGCR, HMGCS, LDLR, FDPS, SS, ACC, FAS, SCD-1 and GPAT, but also ameliorated gene expression in SREBP pathway, including SREBP-1a, SREBP-1c, SREBP-2 and Insig-1,without change in Scap expression (Fig. 6b).
	0.91	HMGCR, HMGCS, LDLR, FDPS (farnesyl diphosphate synthase), SS, FAS (FA synthase), SCD-1 (stearoyl CoA desaturase-1), ACC (acetyl CoA carboxylase), ACLY (ATP citrate lyase), GPAT (glycerol-3-phosphate acyltransferase), SREBP-1c, SREBP-2, and Insig-1 were all lower in PAQR3-shRNA group than in the control mice.
22441164	0.98	3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGCR) is achieved through Insig-1-dependent proteasomal degradation, which also responds to cholesterol levels in the ER.
	0.97	HMGCR, FPPS, IDI1, SQS, squalene epoxidase (SQLE), lanosterol synthase (LSS), 7-dehydrocholesterol reductase (DHCR7), LDL receptor (LDLR) and Insig-1 were all significantly increased 1.6- to 4.7-fold in P0 129 Pex2-/- versus control mouse liver.
28808191	0.98	HMGCR and INSIG1 is dependent on the presence and binding of an oxysterol, such as 25-hydroxycholesterol, to each protein.
	0.98	HMGCR and INSIG1 (lowering endogenous synthetic levels of cholesterol), stimulate the expression of IDOL to degrade LDLR, and stimulate the expression of ABCA1/ABCG1 to promote cholesterol removal from the cell, thereby acting as an effective foil to the SREBP2 pathway.
31953408	0.98	Insulin-induced gene (Insig)-1 and Insig-2, two closely related ER membrane proteins, are key negative regulators controlling lipid biosynthesis and uptake through acting on the sterol-regulated maturation of sterol regulatory element-binding proteins (SREBPs) and degradation of HMG-CoA reductase (HMGCR).
	0.97	Insig-1, as well as the genes involved in cholesterol synthesis (Hmgcr and farnesyl diphosphate synthase [Fds]) and fatty acid and triglyceride (TG) synthesis (fatty acid synthase [Fas], acetyl-CoA carboxylase [Acc], stearoyl-CoA desaturase-1 [Scd-1], glycerol-3-phosphate acyltransferase [Gpat]) were all significantly downregulated in the liver of gp78-/- mice (Fig. 1b).
18618086	0.98	HMG-CoA reductase, modulates the interaction of INSIG-1 with SCAP and HMG-CoA-reductase, is covalently linked to the Hedgehog protein, and binds to synaptophysin and caveolin.
25275627	0.98	Insig1, a regulator of cholesterol biosynthesis through SREBP in both the hearts and WAT of RD fed mice is also responsible for an increased HMGCR expression and cholesterol biosynthesis.
26315393	0.98	HMGCR, HMGCS1, DHCR7, LDLR, ABCA1, and INSIG1.
26634251	0.98	Hmgcr, Insig-1, and Srebp-2 by FGF19 treatment was nearly abolished when SREBP-2 was downregulated in hepatocytes (Fig. 6f), indicating that SHP occupancy is dependent on SREBP-2.
26968099	0.98	insulin-induced gene 1 (INSIG1), a negative regulator of SREBP and HMGCR activities.
27582413	0.98	Insig-1 to the sterol-sensing domain of HMG-CoA reductase accelerates the degradation of this rate-limiting enzyme in cholesterol biosynthesis.
28178673	0.98	INSIG1 protein recruits the reductase that promotes degradation of HMGCR and inhibits cholesterol synthesis.
28720595	0.98	Insig1 reduces transcriptional activity and promotes degradation of key enzymes involved in cholesterol biosynthesis like HMG-CoA reductase.
31934493	0.98	INSIG1 and INSIG2) are endoplasmic reticulum (ER) retention proteins that play roles in both the regulation of the activity of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and the translocation of the sterol regulatory element-binding protein (SREBP) to the nucleus for gene regulation.
30510211	0.97	HMGCR protein consists of two domains: (1) the cytoplasmic C-terminal domain conferring all of the catalytic activity of the enzyme and (2) the membrane-bound domain that interacts with ER-anchored Insig-1 and Insig-2 when cellular sterol accumulates.
	0.97	HMGCR and Insig-1, Cmpd 81 also caused a markedly increase in the ubiquitination of transfected HMGCR (Fig. 5e), accompanied by a reduction of the protein level (Fig. 5f).
	0.94	Insig-1/-2 both completely abrogates the ability of Cmpd 81 to stimulate HMGCR degradation (Fig. 5f, g).
	0.86	HMGCR was completely abolished in SRD-15 cells lacking Insig-1 and Insig-2 proteins (Fig. 5g).
27987056	0.97	HMGCR), HMG-coA synthase (HMGCS), and insulin induced gene 1 (Insig1), were significantly reduced in HFD fed infected mice (4- to 5-fold) compared to RD fed uninfected mice.
	0.96	HMG coA reductase (HMGCR), HMG coA synthase (HMGCS) and Insulin induced gene (Insig1) were significantly decreased in the infected HFD fed mice compared to the infected RD fed mice.
24677249	0.97	Insig1 and reduction in SREBP1c, SREBP2 and HMGCR in the livers of HFD-treated mice (Fig. 5G).
19260826	0.96	HMG-CoA reductase (Hmgcr), the LDL receptor (Ldlr) and Insig1 were lower in 25HC-treated cells than in controls (Figure 4B).
	0.96	Hmgcr, Ldlr and Insig1 expression (Supplementary Figure S2).
	0.96	Hmgcr and Insig1, and both returned to control levels by 8 h after lovastatin removal.
	0.95	Hmgcr, Ldlr and Insig1 mRNA levels (Figure 4B), although less potently than 25HC.
27977712	0.95	3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr; fold change, 2.5), hydroxysteroid (17-beta) dehydrogenase 7 (Hsd17b7; fold change, 2.8), insulin induced gene 1 (Insig1; fold change, 1.8), sterol-C4-methyl oxidase-like (Sc4mol; fold change, 4.5), and leptin receptor (Lepr; fold change, 1.6) were upregulated.
	0.81	Hmgcr, and Insig1) and fatty acid beta-oxidation (Acsl3), whereas it significantly downregulated expression of genes related to fatty acid biosynthesis (Scd1, Acot11, and Mlxipl/carbohydrate responsive element-binding protein [ChREBP]), triacylglycerol biosynthesis (Mogat1), oxidative stress (growth differentiation factor 15, Gdf15), inflammatory and immune processes (Cfd, Chi3l1, Ctse, Orm2, Rorc, and Tlr5), ceramide biosynthesis (Sptlc3), and lipid storage (Plin4).
19691840	0.94	Hmgcr, Insig1 and Sqle while expression of Cyp51a1 and Srebp2 remained unchanged.
	0.66	Hmgcr, Sqle and Insig1 promoters was performed to search for potential CAR binding sites.
28483861	0.51	HMG-CoA reductase (Tobert 2003) and the Insig1 and Insig2 genes were unaltered by the HFD (Table 3).