R&D Systems代理475-WN-005 Recombinant Mouse Wnt-4 Protein (5 UG)

2025-06-28

货号:475-WN-005

品牌:R&D Systems

规格:5ug

目录价:¥4490.00

市场价格:¥3592.00

会员价格:¥3592.00

  • 到货时间:3~4周

    金山科研平台,产品价格货期咨询微信:jinshanbio Source:Chinese Hamster Ovary cell line, CHO-derived, Ser23-Arg351 Accession #:NP_033549 N-terminal Sequence Analysis:Ser23 Purity:>60%, by SDS-PAGE under reducing conditions and visualized by silver stain. Predicted Molecular Mass:36.6 kDa SDS-PAGE:43 kDa, reducing conditions Activity:Measured by its ability to induce alkaline phosphatase production by MC3T3‑E1 mouse preosteoblast cells. Nakamura, K. et al. (1999) Exp. Cell Res. 250:351.The ED50 for this effect is 15 - 60 ng/mL. Molecule Information: Wnt-4 Long Name: Wingless-type MMTV Integration Site Family, Member 4 Entrez Gene IDs: 54361 (Human); 22417 (Mouse) Background: Wnt-4

    View Wnt-4 IHC images. Wnt-4 is a 38 - 42 kDa member of the Wnt family of secreted glycoproteins, which act as short-range signaling molecules via Frizzled receptors and a cascade of intracellular signals in vertebrate embryogenesis. Wnt-4 has been shown to play a critical role in the development of the reproductive system and in the formation of the kidneys, adrenals, pituitary gland, and mammary tissues. In the development of the reproductive system, Wnt-4 expression is down-regulated in the developing gonad after E11.5, although it persists in the developing ovary. Targeted deletion of Wnt-4 results in masculinization of XX mice, with rudimentary development of the masculine internal (Wolffian) ducts and degeneration of the female (Mullerian) reproductive tract. In addition to its involvement in urogenital development, Wnt-4 is also expressed in the perichondrium of the long bones, and promotes osteoblast differentiation. Wnt-4 may also be associated with abnormal proliferation in human breast tissue.

    In humans, mutations in Wnt-4 are the cause of SERKAL syndrome, a syndrome consisting of female to male sex reversal, renal, adrenal, and lung dysgenesis, and developmental defects. Mutations in Wnt-4 also result in Rokitansky-Kuster-Hauser syndrome, which is characterized by utero-vaginal atresia in otherwise phenotypically normal females with normal 46, XX karyotype.

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