Description

  • Product name

    Recombinant human TGF beta Receptor I protein
    See all TGF beta Receptor I proteins and peptides
  • Biological activity

    The Specific activity of ab105908 was determined to be 3 nmol/min/mg.
  • Purity

    > 90 % Densitometry.
    Purity was determined to be >90% by densitometry.
  • Expression system

    Baculovirus infected Sf9 cells
  • Accession

  • Protein length

    Protein fragment
  • Animal free

    No
  • Nature

    Recombinant
    • Species

      Human
    • Predicted molecular weight

      66 kDa including tags
    • Amino acids

      80 to 503
    • Tags

      GST tag N-Terminus

Associated products

Specifications

Our Abpromise guarantee covers the use of ab105908 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    Functional Studies

    Western blot

  • Form

    Liquid
  • Additional notes

    ab204884 (Smad3 peptide) can be utilized as a substrate for assessing kinase activity

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.

    pH: 7.50
    Constituents: 0.307% Glutathione, 0.00174% PMSF, 0.00385% DTT, 0.79% Tris HCl, 0.00292% EDTA, 25% Glycerol, 0.87% Sodium chloride

    This product is an active protein and may elicit a biological response in vivo, handle with caution.

General Info

  • Alternative names

    • AAT 5
    • AAT5
    • Activin A receptor type II like kinase
    • Activin A receptor type II like kinase 53kDa
    • Activin A receptor type II like kinase, 53kD
    • Activin A receptor type II like protein kinase of 53kD
    • activin A receptor type II-like kinase, 53kDa
    • activin A receptor type II-like protein kinase of 53kD
    • Activin receptor like kinase 5
    • Activin receptor-like kinase 5
    • ACVRLK 4
    • ACVRLK4
    • ALK 5
    • ALK-5
    • ALK5
    • LDS1A
    • LDS2A
    • MSSE
    • Serine/threonine protein kinase receptor R4
    • Serine/threonine-protein kinase receptor R4
    • SKR 4
    • SKR4
    • TbetaR I
    • TbetaR-I
    • TGF beta receptor type 1
    • TGF beta receptor type I
    • TGF beta type I receptor
    • TGF-beta receptor type I
    • TGF-beta receptor type-1
    • TGF-beta type I receptor
    • TGFBR 1
    • TGFBR1
    • TGFBR1 protein
    • TGFR 1
    • TGFR-1
    • TGFR1
    • TGFR1_HUMAN
    • Transforming growth factor beta receptor 1
    • Transforming growth factor beta receptor I
    • Transforming growth factor beta receptor I (activin A receptor type II like kinase, 53kD)
    • transforming growth factor, beta receptor 1
    • transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kD)
    • Transforming growth factor-beta receptor type I
    see all
  • Function

    On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for TGF-beta.
  • Tissue specificity

    Found in all tissues examined, most abundant in placenta and least abundant in brain and heart.
  • Involvement in disease

    Defects in TGFBR1 are the cause of Loeys-Dietz syndrome type 1A (LDS1A) [MIM:609192]; also known as Furlong syndrome or Loeys-Dietz aortic aneurysm syndrome (LDAS). LDS1 is an aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by arterial tortuosity and aneurysms, craniosynostosis, hypertelorism, and bifid uvula or cleft palate. Other findings include exotropy, micrognathia and retrognathia, structural brain abnormalities, intellectual deficit, congenital heart disease, translucent skin, joint hyperlaxity and aneurysm with dissection throughout the arterial tree.
    Defects in TGFBR1 are the cause of Loeys-Dietz syndrome type 2A (LDS2A) [MIM:608967]. LDS2 is an aortic aneurysm syndrome with widespread systemic involvement. Physical findings include prominent joint laxity, easy bruising, wide and atrophic scars, velvety and translucent skin with easily visible veins, spontaneous rupture of the spleen or bowel, diffuse arterial aneurysms and dissections, and catastrophic complications of pregnancy, including rupture of the gravid uterus and the arteries, either during pregnancy or in the immediate postpartum period. LDS2 is characterized by the absence of craniofacial abnormalities with the exception of bifid uvula that can be present in some patients.
    Defects in TGFBR1 are the cause of aortic aneurysm familial thoracic type 5 (AAT5) [MIM:608967]. Aneurysms and dissections of the aorta usually result from degenerative changes in the aortic wall. Thoracic aortic aneurysms and dissections are primarily associated with a characteristic histologic appearance known as 'medial necrosis' in which there is degeneration and fragmentation of elastic fibers, loss of smooth muscle cells, and an accumulation of basophilic ground substance.
  • Sequence similarities

    Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.
    Contains 1 GS domain.
    Contains 1 protein kinase domain.
  • Post-translational
    modifications

    Phosphorylated at basal levels in the absence of ligand binding. Activated by multiple phosphorylation, mainly in the GS region.
  • Cellular localization

    Membrane.
  • Information by UniProt

Images

  • The specific activity of TGF beta Receptor I (ab105908) was determined to be 25 nmol/min/mg as per activity assay protocol and was equivalent to 2.5 nmol/min/mg as per radiometric assay
  • SDS PAGE analysis of ab105908
  • SDS PAGE analysis of ab105908
  • Kinase Assay demonstrating specific activity of ab105908 at 3 nmol/min/mg.
  • SDS-PAGE showing ab105908 at approximately 66kDa.

References

ab105908 has not yet been referenced specifically in any publications.

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