LENG8 antibodies are validated for multiple applications across species:
LENG8 associates with the TREX/THO complex, facilitating mRNA nuclear export. Depletion causes nuclear accumulation of poly(A)+ RNA (~59.5% of transcripts affected) .
Binds mitochondrial protein-encoding mRNAs (e.g., VDAC1, VDAC2). Knockdown reduces cytosolic VDAC1 mRNA by 60% .
LENG8 depletion disrupts mitochondrial ultrastructure and respiration. Conditional deletion in murine adipose tissue increases thermogenesis and reduces body weight .
| Interacting Partners | Functional Role |
|---|---|
| THOC1, THOC5, ALYREF (TREX) | mRNA export complex assembly |
| SFPQ, NONO (paraspeckles) | Pre-mRNA splicing and processing |
| PCID2 | Nuclear RNA retention regulation |
| Vendor | Clone | Immunogen Region | Host | Applications |
|---|---|---|---|---|
| Thermo Fisher | 13336-1-AP | 501–800 aa | Rabbit | WB, FC |
| Abcam | ab230864 | 450–700 aa | Rabbit | WB, IHC-P |
| Proteintech | 13336-1-AP | Full-length fusion | Rabbit | WB, FC, ELISA |
Western Blot: Distinct bands at 86–88 kDa in human fetal heart and kidney lysates .
IHC-P: Strong cytoplasmic staining in prostate and thymus tissues .
Specificity: RNA-dependent interactions confirmed via RNase treatment (e.g., THOC1/5 binding loss post-RNase) .
LENG8’s role in mRNA export links transcriptional regulation to mitochondrial health. Its deficiency triggers nuclear retention of critical mRNAs, impairing mitochondrial respiration and activating stress pathways like autophagy . These findings position LENG8 as a potential therapeutic target for metabolic disorders.