FEZ1 (D9R8Q) Rabbit mAb #42480
- WB
- IP
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 65 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:100 |
Storage
Protocol
Specificity / Sensitivity
FEZ1 (D9R8Q) Rabbit mAb recognizes endogenous levels of total FEZ1 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human FEZ1 protein.
Background
The coiled-coil containing protein fasciculation and elongation protein zeta-1 (FEZ1) is expressed predominately in the brain and is the mammalian ortholog of the C. elegans protein UNC-76. It was identified independently in several interaction screens using distinct baits and was shown to play a role in neuronal differentiation and outgrowth, viral defense, centrosome organization, cytoskeletal signaling, and autophagy (reviewed in 1). It was originally identified as a binding partner and substrate for PKCζ and was found to induce the neuronal differentiation of PC-12 cells when co-expressed with active PKCζ (2). FEZ1 was also found to be an interacting partner with the schizophrenia-associated protein DISC1, which may suggest a role for FEZ1 in schizophrenia as well as other mental disorders (3,4). FEZ1 has also been shown to bind to several cytoskeletal proteins, including kinesins, tubulins, JIP1, NEK1, and CLASP2, which supports its role in neurite outgrowth, cargo transport along microtubules, and centrosomal organization (5-7). Additional research studies have shown that FEZ1 interacts with a viral agnoprotein and plays a role in viral defense, including during HIV-1 infection (8-10). Another screen identified FEZ1 as a binding partner for the ubiquitin ligase E4B and showed that FEZ1 can be regulated through polyubiquitination (11). Moreover, degradation of FEZ1 by the ubiquitination-proteasomal pathway through cdc20 provides a mechanism for FEZ1 in dendritic outgrowth (12). FEZ1 was also found to regulate autophagy through association with ULK1 and Beclin-1 complexes (13).
Limited Uses
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