research use only
Cat.No.: F2605
| Dilution |
|---|
|
| Application |
|---|
| WB |
| Reactivity |
|---|
| Human |
| Source |
|---|
| Rabbit Monoclonal Antibody |
| Storage Buffer |
|---|
| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
|---|
| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
|---|
| 50-100 kDa 55 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. |
| Positive Control | IMR-32 cells; SH-SY5Y cells (Okadiac acid and calyculin A treated) |
|---|---|
| Negative Control | SH-SY5Y cells; IMR-32 (phosphatase treated) |
| Specificity |
|---|
| Phospho-Tau (Ser422) Antibody [L19H1] detects endogenous levels of total Tau protein only when it is phosphorylated at Ser422. |
| Clone |
|---|
| L19H1 |
| Synonym(s) |
|---|
| MAPT; Microtubule-associated protein tau; Neurofibrillary tangle protein; Paired helical filament-tau; PHF-tau |
| Background |
|---|
| Phospho-Tau (Ser422) is a disease-associated post-translational modification of the microtubule-associated protein Tau (MAPT), one of six brain isoforms (~352–441 aa) that normally stabilizes axonal microtubules via its N-terminal projection domain, proline-rich region (P1/P2 motifs), four microtubule-binding repeats (R1–R4), and C-terminal tail. Ser422 resides in the R2 repeat flanking the KXGS motifs critical for tubulin binding; phosphorylation at pSer422 (mimicked by S422E pseudophosphorylation) enhances SDS-stable dimer formation, prolongs aggregation nucleation, exposes the phosphatase-activating domain (PAD, aa 2-18), and alters tau conformers without changing total aggregate yield. pSer422 tau monomers inhibit anterograde kinesin-1-dependent fast axonal transport (FAT), while its aggregates uniquely block both anterograde and retrograde FAT, unlike unmodified tau, disrupting axonal trafficking of vesicles, mitochondria, and signaling molecules essential for neuronal viability. This modification correlates with cognitive decline, neuropil threads, and oligomeric tau in prodromal Alzheimer's disease (AD) brain, activating PP1-GSK3β pathways that exacerbate microtubule disassembly, synaptic loss, and neurodegeneration in tauopathies. |
| References |
|---|
|
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.