ActiveMax® Human Flt-3 Ligand Protein, Tag Free

Source : 

ActiveMax® Human Flt-3 Ligand, Tag Free (FLL-H5218) is expressed from human 293 cells (HEK293). It contains AA Thr 27 - Pro 185 (Accession # AAI26294).

 

Molecule : Flt-3 Ligand

 

Synonyms : FLT3LG,FL,FLT3L,Flt3 ligand

 

Format : Powder

 

Category : ActiveMax® Cytokines

 

Accession : AAI26294

 

Storage : -20℃

 

Shipping condition : Powder,RT

 

Molecular Weight : 18.0 kDa

 

Characteristics :

This protein carries no "tag". The protein has a calculated MW of 18.0 kDa. The protein migrates as 25-30 kDa under reducing (R) condition (SDS-PAGE).

 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.

 

Buffer : PBS, pH7.4

 

Description :

FMS-like tyrosine kinase 3 ligand (Flt-3 Ligand) is also known as FL, Flt3L and FLT3LG, is an α-helical cytokine that promotes the differentiation of multiple hematopoietic cell lineages. FLT3LG is expressed as a noncovalentlylinked dimer by T cells and bone marrow and thymic fibroblasts. Each 36 kDa chain carries approximately 12 kDa of N- and O- linked carbohydrates. FLT3LG is structurally homologous to stem cell factor (SCF) and colony stimulating facor 1 (CSF-1). FLT3LG acts as a growth factor that increases the number of immune cells by activating the hematopoietic progenitors. It also induces the mobilization of the hematopoietic progenitors and stem cells in vivo which may help the system to kill cancer cells. FLT3LG induces the expansion of monocytes and immature dendritic cells as well as early B cell lineage differentiation. FLT3LG cooperates with IL2, IL6, IL7, and IL15 to induce NK cell development and with IL3, IL7 and IL11 to induce terminal B cell maturation. Animal studies also show FLT3LG to reduce the severity of experimentally induced allergic inflammation. FLT3LG is crucial for steady-state pDC and cDC development. A lack of FLT3L results in low levels of DCs.

 

References :

(1) Wodnar-Filipowicz A., 2003, News Physiol Sci., 18:247-51.
(2) McClanahan T., et al., 1996, Blood, 88(9):3371-82.
(3) Diener K.R. et al., 2008, Exp Hematol., 36(1):51-60.
(4) Farag SS, Caligiuri MA, 2006, Blood Rev. 20(3):123-37.
(5) Shortman, Ken, et al., 2006, Nature Reviews Immunology 7 (1): 19–30.