General Information of the Molecule (ID: Mol01916)
Name
Sterol O-acyltransferase 1 (SOAT1) ,Homo sapiens
Synonyms
SOAT1; ACACT; ACACT1; ACAT; ACAT1; SOAT; STAT
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Molecule Type
Protein
Gene Name
SOAT1
Gene ID
6646
Location
chr1:179,293,714-179,358,680[+]
Sequence
MVGEEKMSLRNRLSKSRENPEEDEDQRNPAKESLETPSNGRIDIKQLIAKKIKLTAEAEE
LKPFFMKEVGSHFDDFVTNLIEKSASLDNGGCALTTFSVLEGEKNNHRAKDLRAPPEQGK
IFIARRSLLDELLEVDHIRTIYHMFIALLILFILSTLVVDYIDEGRLVLEFSLLSYAFGK
FPTVVWTWWIMFLSTFSVPYFLFQHWATGYSKSSHPLIRSLFHGFLFMIFQIGVLGFGPT
YVVLAYTLPPASRFIIIFEQIRFVMKAHSFVRENVPRVLNSAKEKSSTVPIPTVNQYLYF
LFAPTLIYRDSYPRNPTVRWGYVAMKFAQVFGCFFYVYYIFERLCAPLFRNIKQEPFSAR
VLVLCVFNSILPGVLILFLTFFAFLHCWLNAFAEMLRFGDRMFYKDWWNSTSYSNYYRTW
NVVVHDWLYYYAYKDFLWFFSKRFKSAAMLAVFAVSAVVHEYALAVCLSFFYPVLFVLFM
FFGMAFNFIVNDSRKKPIWNVLMWTSLFLGNGVLLCFYSQEWYARQHCPLKNPTFLDYVR
PRSWTCRYVF
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3D-structure
PDB ID
6P2J
Classification
Transferase
Method
Electron microscopy
Resolution
3.00  Å
Function
Catalyzes the formation of fatty acid-cholesterol esters, which are less soluble in membranes than cholesterol. Plays a role in lipoprotein assembly and dietary cholesterol absorption. Utilizes oleoyl-CoA ((9Z)-octadecenoyl-CoA) preferentially as susbstrate: shows a higher activity towards an acyl-CoA substrate with a double bond at the delta-9 position (9Z) than towards saturated acyl-CoA or an unsaturated acyl-CoA with a double bond at the delta-7 (7Z) or delta-11 (11Z) positions.
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Uniprot ID
SOAT1_HUMAN
Ensembl ID
ENSG00000057252
HGNC ID
HGNC:11177
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Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
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Fluvastatin
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
  Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Disease Class: Breast cancer [ICD-11: 2C60.3] [1]
Resistant Disease Breast cancer [ICD-11: 2C60.3]
Resistant Drug Fluvastatin
Molecule Alteration Expression
Up-regulation
Differential expression of the molecule in resistant disease
Classification of Disease Breast cancer [ICD-11: 2C60]
The Specified Disease Breast cancer
The Studied Tissue Breast tissue
The Expression Level of Disease Section Compare with the Healthy Individual Tissue
p-value: 2.41E-33
Fold-change: 1.47E-01
Z-score: 1.31E+01
Experimental Note Discovered Using In-vivo Testing Model
Cell Pathway Regulation Steroid biosynthesis signaling pathway Activation hsa00100
Terpenoid bacKbone biosynthesis signaling pathway Activation hsa00900
Steroid hormone biosynthesis signaling pathway Activation hsa00140
In Vitro Model MCF-10A-neoT cells Breast Homo sapiens (Human) CVCL_5554
In Vivo Model SV40 C3TAg transgenic mouse model Mus musculus
Experiment for
Molecule Alteration
Clariom D RNA profiling assay
Experiment for
Drug Resistance
MTT assay; Colony formation assay
Mechanism Description Acquired resistance to fluvastatin is mediated by restorative upregulation of cholesterol biosynthesis pathway genes.
Disease- and Tissue-specific Abundances of This Molecule
ICD Disease Classification 02
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Breast cancer [ICD-11: 2C60]
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Differential expression of molecule in resistant diseases
The Studied Tissue Breast tissue
The Specified Disease Breast cancer
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 2.41E-33; Fold-change: 7.28E-01; Z-score: 9.03E-01
The Expression Level of Disease Section Compare with the Adjacent Tissue p-value: 5.37E-08; Fold-change: 6.66E-01; Z-score: 9.54E-01
Molecule expression in the normal tissue adjacent to the diseased tissue of patients
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Tissue-specific Molecule Abundances in Healthy Individuals
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References
Ref 1 Gene signature associated with resistance to fluvastatin chemoprevention for breast cancer .BMC Cancer. 2022 Mar 17;22(1):282. doi: 10.1186/s12885-022-09353-2. 10.1186/s12885-022-09353-2

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