ZIP14/SLC39A14 (E3H7D) Rabbit mAb #24161
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 55-65 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunofluorescence (Immunocytochemistry) | 1:800 - 1:1600 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
The reported ZIP14 L441R mutation (L438R in mice) disrupts plasma membrane presentation of the transporter, causing intracellular accumulation of zinc in osteoblasts, characterized by excessive bone overgrowth (4).
SLC39A14 mutation or knockdown can cause manganese dyshomeostasis, resulting in childhood-onset dystonia-Parkinsonism (5). The activity of liver-expressed ZIP14/SLC39A14, intestinal SLC39A10, and blood-brain barrier ZIP8/SLC39A8 all contribute to manganese homeostasis during neuronal development (6,7).
- Zhao, N. et al. (2010) J Biol Chem 285, 32141-50.
- McCabe, S. et al. (2023) Comput Struct Biotechnol J 21, 2332-2338.
- Maxel, T. et al. (2019) Sci Rep 9, 8589.
- Hendrickx, G. et al. (2018) PLoS Genet 14, e1007321.
- Tuschl, K. et al. (2016) Nat Commun 7, 11601.
- Hutchens, S. et al. (2023) Am J Physiol Gastrointest Liver Physiol 325, G251-G264.
- Liu, Q. et al. (2023) J Biol Chem 299, 105078.
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