FAM92A antibodies are polyclonal rabbit IgG antibodies developed against specific epitopes of the FAM92A1 protein (also known as CIBAR1). Two commercially available variants include:
These antibodies are validated for techniques such as Western blot (WB), immunohistochemistry (IHC), and immunofluorescence (IF/ICC) .
FAM92A antibodies have been instrumental in:
Localization Studies: Identifying FAM92A at centrioles/basal bodies during ciliogenesis and synapses in neuronal tissues .
Functional Knockdown: Demonstrating that FAM92A depletion impairs primary cilia formation in retinal pigment epithelial (RPE1) cells .
Disease Modeling: Linking FAM92A loss-of-function variants to nonsyndromic postaxial polydactyly in humans and skeletal abnormalities in mice .
Structural Analysis: Revealing FAM92A's BAR domain interactions with phosphoinositides and cardiolipin for membrane curvature induction .
FAM92A antibodies confirmed its interaction with Chibby1 (Cby1), a protein critical for basal body docking during cilia formation. Knockdown of FAM92A disrupts Rab8-positive membrane structures necessary for ciliogenesis .
In FAM92A1 knockout mice, these antibodies revealed:
Reduced gray matter density in the entorhinal cortex and hippocampus .
Abnormal mitochondrial cristae, synaptic ultrastructure, and myelin sheath integrity .
Age-dependent cognitive deficits linked to impaired synaptic plasticity .
A FAM92A frameshift mutation (c.490delC) was associated with polydactyly via disrupted ciliary localization of FAM92A and Cby1 .
Specificity: The Proteintech antibody (24803-1-AP) loses reactivity in FAM92A1 knockout mice due to epitope deletion, whereas Sigma HPA034760 retains binding to residual exons 7–8 sequences .
Validation: Both antibodies show orthogonal RNAseq validation but differ in non-specific band profiles during Western blotting .
Experimental Design: Researchers must select antibodies based on target epitopes, especially when studying FAM92A1 knockout models .