Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Alexa Fluor® 647 Rabbit monoclonal [EP1573Y] to Stathmin 1
- Suitable for: ICC/IF
- Reacts with: Mouse
- Conjugation: Alexa Fluor® 647. Ex: 652nm, Em: 668nm
Product nameAlexa Fluor® 647 Anti-Stathmin 1 antibody [EP1573Y]
See all Stathmin 1 primary antibodies
DescriptionAlexa Fluor® 647 Rabbit monoclonal [EP1573Y] to Stathmin 1
ConjugationAlexa Fluor® 647. Ex: 652nm, Em: 668nm
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Mouse
Predicted to work with: Rat, Human
Synthetic peptide within Human Stathmin 1 aa 100 to the C-terminus (C terminal). The exact sequence is proprietary.
Database link: P16949
- ICC/IF: Neuro2a cells.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle. Store In the Dark.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 30% Glycerol, 1% BSA
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab199812 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
This product gave a positive signal in Neuro2a cells fixed with 4% formaldehyde (10 min).
FunctionInvolved in the regulation of the microtubule (MT) filament system by destabilizing microtubules. Prevents assembly and promotes disassembly of microtubules. Phosphorylation at Ser-16 may be required for axon formation during neurogenesis. Involved in the control of the learned and innate fear.
Tissue specificityUbiquitous. Expression is strongest in fetal and adult brain, spinal cord, and cerebellum, followed by thymus, bone marrow, testis, and fetal liver. Expression is intermediate in colon, ovary, placenta, uterus, and trachea, and is readily detected at substantially lower levels in all other tissues examined. Lowest expression is found in adult liver. Present in much greater abundance in cells from patients with acute leukemia of different subtypes than in normal peripheral blood lymphocytes, non-leukemic proliferating lymphoid cells, bone marrow cells, or cells from patients with chronic lymphoid or myeloid leukemia.
Sequence similaritiesBelongs to the stathmin family.
Contains 1 SLD (stathmin-like) domain.
modificationsMany different phosphorylated forms are observed depending on specific combinations among the sites which can be phosphorylated. MAPK is responsible for the phosphorylation of stathmin in response to NGF. Phosphorylation at Ser-16 seems to be required for neuron polarization (By similarity). Phosphorylation at Ser-63 reduces tubulin binding 10-fold and suppresses the MT polymerization inhibition activity.
Cellular localizationCytoplasm > cytoskeleton.
- Information by UniProt
- C1orf215 antibody
- Lag antibody
- LAP 18 antibody
ab199812 staining Stathmin 1 in Neuro2a cells. The cells were fixed with 4% formaldehyde (10 min), permeabilized with 0.1% Triton X-100 for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1% PBS-Tween for 1h. The cells were then incubated overnight at +4°C with ab199812 at 1/200 dilution (shown in red) and ab195887, Mouse monoclonal to alpha Tubulin (Alexa Fluor® 488), at 1/250 dilution (shown in green). Nuclear DNA was labelled with DAPI (shown in blue).
Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).
ab199812 has not yet been referenced specifically in any publications.