ier3ip1 Antibody

Overview of IER3IP1 Antibody

IER3IP1 antibodies are polyclonal or monoclonal reagents designed to detect IER3IP1, an 82-amino acid protein with two transmembrane domains . These antibodies are critical for studying IER3IP1’s roles in:

• ER-to-Golgi trafficking

• Unfolded protein response (UPR) modulation

• β-cell apoptosis and proliferation

• B cell development and function

Validated antibodies include Proteintech 29402-1-AP (rabbit polyclonal) and Sigma-Aldrich HPA010027 (rabbit polyclonal), both targeting human IER3IP1 .

Immunohistochemistry (IHC)

• Proteintech: Detects IER3IP1 in human kidney tissue with antigen retrieval (TE buffer pH 9.0) .

• Sigma-Aldrich: Validated across 44 normal and 20 cancerous human tissues via the Human Protein Atlas .

Western Blot (WB)

• Confirmed in A549 and HeLa cell lysates (9 kDa band) .

• Used to quantify IER3IP1 knockdown efficiency in MIN6 β-cells and HeLa KO models .

Immunofluorescence (IF)

• Localizes IER3IP1 to ER exit sites (ERES) and ER-Golgi intermediate compartments (ERGIC) in U2OS and HeLa cells .

B Cell Development

• Role: IER3IP1 deficiency in mice (alarmist mutants) disrupts B cell maturation at the pre-pro-B stage, reducing serum immunoglobulins (IgG, IgA) .

• Mechanism: Antibody staining revealed impaired LPS-induced class-switch recombination and cell cycle arrest .

β-Cell Dysfunction in Diabetes

• Apoptosis: IER3IP1 knockdown in MIN6 cells increased cleaved caspase-3 (3-fold) and PARP .

• UPR Suppression: Reduced IRE1α phosphorylation and sXBP-1 levels were detected via WB .

ER Trafficking Defects

• SC-islet Models: CRISPR-edited IER3IP1 mutant β-cells showed 3x slower proinsulin trafficking to Golgi .

• Secretory Pathway: IER3IP1 KO HeLa cells exhibited aberrant ER chaperone (BiP, calreticulin) secretion .

Limitations and Considerations

• Specificity: Cross-reactivity with homologous proteins (e.g., TMEM167A) requires validation via KO controls .

• Storage: Proteintech antibodies require -20°C storage with 50% glycerol .