FSTL3 (Protein | Antibody | cDNA Clone | ELISA Kit)

All FSTL3 reagents are produced in house and quality controlled, including 4 FSTL3 Antibody, 15 FSTL3 Gene, 1 FSTL3 Lysate, 1 FSTL3 Protein, 1 FSTL3 qPCR. All FSTL3 reagents are ready to use.

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FSTL3 Background

Follistatin-like 3 (FLRG/Fstl3) is a secreted glycoprotein of the follistatin-module-protein family. It may have a role in leukemogenesis. FLRG/Fstl3 is a recently described member of the FST family having an overall structure and activity profile similar to that of FST, including binding and neutralization of activin. FLRG/Fstl3 is expressed in a wide range of adult tissues, not detected in hematopoietic cells except in patients with a B cell chronic leukemia and a translocation. Isoform 1 or the secreted form is a binding and antagonizing protein for members of the TGF-beta family, such us activin, BMP2 and MSTN. Inhibits activin A-, activin B-, BMP2- and MSDT-induced cellular signaling; more effective on activin A than on activin B. Involved in bone formation; inhibits osteoclast differentiationc. Involved in hematopoiesis; involved in differentiation of hemopoietic progenitor cells, increases hematopoietic cell adhesion to fibronectin and seems to contribute to the adhesion of hematopoietic precursor cells to the bone marrow stroma. Isoform 2 of FLRG/Fstl3 or the nuclear form of FLRG/Fstl3 is probably involved in transcriptional regulation via interaction with MLLT1. Modulation of activin and other TGFβ superfamily signaling is the primary mechanism of action for both follistatin (FS) and FS-like 3 (FSTL-3). FLRG/Fstl3 is likely to be a local regulator of activin action in gonadal development and gametogenesis and, further, that activin appears to have important actions in gonadal development and function that are critical for normal reproduction.

FSTL3 References

  • Sidis Y, et al. (2006) Biological activity of follistatin isoforms and follistatin-like-3 is dependent on differential cell surface binding and specificity for activin, myostatin, and bone morphogenetic proteins. Endocrinology. 147(7): 3586-97.
  • Schneyer A, et al. (2003) Differential binding and neutralization of activins A and B by follistatin and follistatin like-3 (FSTL-3/FSRP/FLRG). Endocrinology. 144(5): 1671-4.
  • Xia Y, et al. (2004) Overexpression of follistatin-like 3 in gonads causes defects in gonadal development and function in transgenic mice. Mol Endocrinol. 18(4): 979-94.