Przejdź do zawartości
Merck

MABS1697

Anti-WISP-3 Antibody, clone 13C4.1

clone 13C4.1, from mouse

Synonim(y):

WNT1-inducible-signaling pathway protein 3, CCN family member 6, WISP-3

Zaloguj się, aby wyświetlić ceny organizacyjne i kontraktowe.

Wybierz wielkość

Zmień widok

Informacje o tej pozycji

UNSPSC Code:
12352203
NACRES:
NA.43
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
13C4.1, monoclonal
Application:
IHC, WB
Citations:
-
Pomoc techniczna
Potrzebujesz pomocy? Nasz zespół doświadczonych naukowców chętnie Ci pomoże.
Pozwól nam pomóc


biological source

mouse

Quality Segment

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

13C4.1, monoclonal

species reactivity

mouse, human, rat

technique(s)

immunohistochemistry: suitable (paraffin), western blot: suitable

isotype

IgG1κ

NCBI accession no.

UniProt accession no.

shipped in

ambient

target post-translational modification

unmodified

Gene Information

human ... CCN6(8838)

General description

WNT1-inducible-signaling pathway protein 3 (UniProt O95389; also known as CCN family member 6, WISP-3) is encoded by the WISP3 (also known as CCN6, LIBC, PPAC, PPRD, UNQ462/PRO790/PRO956) gene (Gene ID 8838) in human. WISP-3 is a member of the CCN (CTGF, Cyr61, NOV) family connective tissue growth modulators involved in cell growth/differentiation during various phases of development through a complex interplay with BMP/Notch/Wnt signaling pathways. WISP-3 is expressed in cells and tissues of mesenchymal origin and WISP3 gene mutations are linked to an autosomal recessive skeletal disorder known as progressive pseudorheumatoid dysplasia (PPRD), indicating its importance in skeletal growth and the maintenance of cartilage integrity. WISP-3 interacts with BMP and components of the Wnt1 signaling pathway including LRP6 and Fz8, promoting the expression of cartilage-specific proteins collagen-II and aggrecan. Both IGF1 and ROS stimulate WISP-3 expression, WISP-3 in turn binds to and blocks IGF1 secretion, preventing IGF1-induced collagen X induction, ROS accumulation, and alkaline phosphatase activity, all of which are associated with chondrocyte hypertrophy induction. Human WISP-3 is synthesized with a signal peptide sequence (a.a. 1-23), the removal of which yields the mature protein containing several protein-interacting domains, including an IGF-interacting IGFBP domain (a.a. 44-117) with a von Willbrand factor type C repeat, a Thrombospondin (TSP) type-1 domain (a.a. 208-253), and a C-terminal cystine knot-like (CTCK) domain (a.a. 268-342).
~39 kDa observed. 36.84/36.33 kDa (human/rat mature form), 39.29/41.40 kDa (human isoform 1/2 pro-form), and 38.92 kDa (rat pro-form) calculated. Uncharacterized bands may be observed in some lysate(s).

Immunogen

GST-tagged recombinant human WISP-3 IGFBP domain fragment.

Application

Detect WISP-3 using this mouse monoclonal Anti-WISP-3, clone 13C4.1, Cat. No. MABS1697, validated for use in Immunohistochemistry (Paraffin) and Western Blotting.
Immunohistochemistry Analysis: A 1:50-1,000 dilution of this antibody detected WISP-3 in human liver, kidney, and lung tissue sections.

Biochem/physiol Actions

Clone 13C4.1 targets an epitope within the WISP-3 IGFBP domain.

Physical form

Format: Purified

Analysis Note

Evaluated by Western Blotting in rat kidney tissue lysate.

Western Blotting Analysis: A 1:1,000 dilution of this antibody detected WISP-3 in 10 µg of rat kidney tissue lysate.

Other Notes

Concentration: Please refer to lot specific datasheet.
Ta strona może zawierać tekst przetłumaczony maszynowo.


Still not finding the right product?

Wypróbuj nasze narzędzie Narzędzie selektora produktów, aby zawęzić opcje.


Klasa składowania

12 - Non Combustible Liquids

wgk

WGK 1



Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

Masz już ten produkt?

Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów