acly-1 Antibody

Target Overview: ATP-Citrate Lyase (ACLY)

ACLY catalyzes citrate conversion to cytosolic acetyl-CoA, a key metabolite for lipid synthesis and histone acetylation . It is overexpressed in cancers (e.g., nonsmall cell lung carcinoma, hepatocellular carcinoma) and linked to tumor progression via lipid metabolism and epigenetic regulation .

Representative Products

Western Blot (WB)

• Detects endogenous ACLY at 120–125 kDa in human, mouse, and rat lysates .

• Example: Strong signal in K562 and HeLa cells , with reduced detection in ACLY-knockout models .

Immunohistochemistry (IHC)

• Localizes ACLY in hepatocellular carcinoma tissues, showing overexpression compared to normal parenchyma .

Functional Studies

• Cancer Research: ACLY inhibition increases PD-L1 expression, promoting T-cell exhaustion and compromising immunotherapy efficacy .

• Epigenetics: Nuclear ACLY maintains histone H3K27 acetylation, critical for TGFβ-induced fibroblast activation .

Lipid Metabolism & Cancer

• ACLY knockdown suppresses proliferation in pancreatic cancer (Pan02 cells) in vitro but fails to inhibit tumor growth in vivo due to immunosuppressive effects .

• Correlates with poor prognosis in cholangiocarcinoma (CCA); inhibition induces ferroptosis and reduces stemness .

Immune Regulation

• Pro-inflammatory Role: ACLY-deficient macrophages show reduced IL-6 and IL-12p70 in LPS-induced peritonitis models .

• Contradictory Findings: Pharmacological inhibitors (e.g., BMS303141) reduce histone acetylation at high doses, but silencing ACLY does not alter inflammatory cytokine expression in THP-1 cells .

Therapeutic Targeting

• Bempedoic Acid: Liver-targeted ACLY inhibitor reduces LDL cholesterol in hypercholesterolemia .

• Combination Therapy: ACLY inhibition synergizes with anti-PD-L1 immunotherapy in cGAS-dependent tumor models .

Antibody Comparison

Limitations and Considerations

• Cross-Reactivity: Limited to human, mouse, and rat; chicken reactivity is predicted but unverified .

• Inhibitor Specificity: High doses of BMS303141 exhibit off-target effects on histone acetylation .

• Therapeutic Complexity: ACLY inhibition upregulates PD-L1, which may counteract antitumor immunity .