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AB73019

Anti-Flt3 / CD135 antibody [RM0021-12B6]

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(2 Publications)

Rat Monoclonal Flt3 / CD135 antibody. Suitable for IHC-P and reacts with Mouse samples. Cited in 2 publications. Immunogen corresponding to Recombinant Fragment Protein within Mouse Flt3.

View Alternative Names

CD135, Flk-2, Flt-3, Flt3, Receptor-type tyrosine-protein kinase FLT3, FL cytokine receptor, Fetal liver kinase 2, Fms-like tyrosine kinase 3, Tyrosine-protein kinase receptor flk-2, FLK-2, FLT-3

1 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Flt3 / CD135 antibody [RM0021-12B6] (AB73019)
  • IHC-P

Unknown

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Flt3 / CD135 antibody [RM0021-12B6] (AB73019)

ab73019 at 1/100 dilution, staining Flt3 / CD135 in LPS treated mouse tissue section by Immunohistochemistry (Formalin/PFA fixed paraffin-embedded sections).

Key facts

Host species

Rat

Clonality

Monoclonal

Clone number

RM0021-12B6

Isotype

IgG2

Carrier free

No

Reacts with

Mouse

Applications

IHC-P

applications

Immunogen

Recombinant Fragment Protein within Mouse Flt3. The exact immunogen used to generate this antibody is proprietary information.

Q00342

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "IHCP" : {"fullname" : "Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)", "shortname":"IHC-P"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Mouse": { "IHCP-species-checked": "testedAndGuaranteed", "IHCP-species-dilution-info": "1/50 - 1/100", "IHCP-species-notes": "<p></p>" } } }

Properties and storage information

Form
Lyophilized
Reconstitution
reconstitute with PBS at 500µL
Purification technique
Affinity purification Protein G
Purification notes
Purified from tissue culture supernatant.Filter sterilised.
Storage buffer
Constituents: PBS
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Flt3 also known as CD135 or FLT3 tyrosine kinase is a receptor tyrosine kinase that belongs to the class III receptor tyrosine kinase family. It has a molecular weight of approximately 160 kDa. This protein plays an important role in the development of hematopoietic stem and progenitor cells. Flt3 is expressed mainly in early progenitor cells within the bone marrow. Additionally it is present in some populations of mature cells in the peripheral blood and lymphoid organs.
Biological function summary

Flt3 functions as a receptor that is activated by binding to its ligand FLT3 ligand (FLT3L). This interaction stimulates the associated tyrosine kinase activity leading to auto-phosphorylation of Flt3 and subsequent downstream signaling. Flt3 does not form a heterocomplex rather it dimerizes upon ligand binding to initiate signaling cascades. These cascades promote cell proliferation differentiation and survival particularly impacting hematopoiesis and immune responses.

Pathways

Flt3 signaling impacts the internal signaling networks involving the MAPK/ERK and PI3K/AKT pathways both central to cell cycle regulation and apoptosis. Flt3 interacts functionally with proteins such as SHP2 and GRB2 in these pathways aiding signal transduction. The Flt3 receptor also shares functional motifs with KIT and PDGF receptors indicating shared regulatory mechanisms involved in cellular proliferation.

Flt3 mutations especially internal tandem duplications in Flt3/ITD are significant in acute myeloid leukemia (AML) leading to abnormal cell growth and survival. These mutations often co-occur with other genetic anomalies such as NPM1 mutations contributing to the oncogenic process. The abnormal activation of Flt3 kinase activity also has ramifications in myelodysplastic syndromes making it a target for therapeutic intervention with drugs such as anti-FLT3 inhibitors in the treatment regime.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Tyrosine-protein kinase that acts as a cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.
See full target information Flt3

Publications (2)

Recent publications for all applications. Explore the full list and refine your search

Brain : a journal of neurology 143:266-288 PubMed31848580

2019

Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease.

Applications

Unspecified application

Species

Unspecified reactive species

Joshua D Crapser,Joseph Ochaba,Neelakshi Soni,Jack C Reidling,Leslie M Thompson,Kim N Green

Proceedings of the National Academy of Sciences of the United States of America 112:E6644-53 PubMed26627255

2015

Murine germinal center B cells require functional Fms-like tyrosine kinase 3 signaling for IgG1 class-switch recombination.

Applications

IHC

Species

Mouse

Mattias N D Svensson,Karin M E Andersson,Caroline Wasén,Malin C Erlandsson,Merja Nurkkala-Karlsson,Ing-Marie Jonsson,Mikael Brisslert,Mats Bemark,Maria I Bokarewa
View all publications

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