Anti-SHH monoclonal antibody, clone 9H4

Name: Anti-SHH monoclonal antibody, clone 9H4
SKU: DCABH-13432
Rating: 5 (1 reviews)

Mouse anti-Human SHH monoclonal antibody for WB, ELISA

Write a review

COA

SDS

Datasheet

Summary

Specifications

Clone

9H4

Species Reactivity

Human

Immunogen

Recombinant protein corresponding to human SHH.

Conjugate

Unconjugated

Applications

Application Notes

ELISA (1:10000); WB (1:500-1:2000) & The optimal working dilution should be determined by the end user.

Target

Alternative Names

SHH; sonic hedgehog; HLP3, HPE3, sonic hedgehog (Drosophila) homolog , sonic hedgehog homolog (Drosophila); sonic hedgehog protein; HHG1; MCOPCB5; SMMCI; TPT; TPTPS; sonic hedgehog homolog; HLP3; HPE3;

Entrez Gene ID

6469

UniProt ID

Q15465

Product Background

Antigen Description

This gene encodes a protein that is instrumental in patterning the early embryo. It has been implicated as the key inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. Of three human proteins showing sequence and functional similarity to the sonic hedgehog protein of Drosophila, this protein is the most similar. The protein is made as a precursor that is autocatalytically cleaved; the N-terminal portion is soluble and contains the signalling activity while the C-terminal portion is involved in precursor processing. More importantly, the C-terminal product covalently attaches a cholesterol moiety to the N-terminal product, restricting the N-terminal product to the cell surface and preventing it from freely diffusing throughout the developing embryo. Defects in this protein or in its signalling pathway are a cause of holoprosencephaly (HPE), a disorder in which the developing forebrain fails to correctly separate into right and left hemispheres. HPE is manifested by facial deformities. It is also thought that mutations in this gene or in its signalling pathway may be responsible for VACTERL syndrome, which is characterized by vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal dysplasia, cardiac anomalies, and limb abnormalities. Additionally, mutations in a long range enhancer located approximately 1 megabase upstream of this gene disrupt limb patterning and can result in preaxial polydactyly.

Pathway

Basal cell carcinoma, organism-specific biosystem; Basal cell carcinoma, conserved biosystem; Class B/2 (Secretin family receptors), organism-specific biosystem; FOXA1 transcription factor network, organism-specific biosystem; GPCR ligand binding, organism-specific biosystem; Glypican 3 network, organism-specific biosystem; Heart Development, organism-specific biosystem;

Citations

Have you cited DCABH-13432 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Sonic Hedgehog, a Novel Endogenous Damage Signal, Activates Multiple Beneficial Functions of Human Endometrial Stem Cells

MOLECULAR THERAPY

Authors: Park, Se-Ra; Kim, Soo-Rim; Park, Chan Hum; Lim, Soyi; Ha, Seung Yeon; Hong, In-Sun; Lee, Hwa-Yong

Abstract

Local endometrial stem cells play an important role in regulating endometrial thickness, which is an essential factor for successful embryo implantation and pregnancy outcomes. Importantly, defects in endometrial stem cell function can be responsible for thin endometrium and subsequent recurrent pregnancy losses. Therefore, many researchers have directed their efforts toward finding a novel stimulatory factor that can enhance the regenerative capacity of endometrial stem cells. Sonic hedgehog (SHH) is a morphogen that plays a key role in regulating pattern formation throughout embryonic limb development. In addition to this canonical function, we identified for the first time that SHH is actively secreted as a stem cell-activating factor in response to tissue injury and subsequently stimulates tissue regeneration by promoting various beneficial functions of endometrial stem cells. Our results also showed that SHH exerts stimulatory effects on endometrial stem cells via the FAK/ERK1/2 and/or phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways. More importantly, we also observed that endometrial stem cells stimulated with SHH showed markedly enhanced differentiation and migratory capacities and subsequent in vivo therapeutic effects in an endometrial ablation animal model.

Development of the Proximal-Anterior Skeletal Elements in the Mouse Hindlimb Is Regulated by a Transcriptional and Signaling Network Controlled by Sall4

GENETICS

Authors: Chen, Katherine Q.; Tahara, Naoyuki; Anderson, Aaron; Kawakami, Hiroko; Kawakami, Sho; Nishinakamura, Ryuichi; Pandolfi, Pier Paolo; Kawakami, Yasuhiko

Abstract

The vertebrate limb serves as an experimental paradigm to study mechanisms that regulate development of the stereotypical skeletal elements. In this study, we simultaneously inactivated Sall4 using Hoxb6Cre and Plzf in mouse embryos, and found that their combined function regulates development of the proximal-anterior skeletal elements in hindlimbs. The Sall4; Plzf double knockout exhibits severe defects in the femur, tibia, and anterior digits, distinct defects compared to other allelic series of Sall4; Plzf. We found that Sall4 regulates Plzf expression prior to hindlimb outgrowth. Further expression analysis indicated that Hox10 genes and GLI3 are severely downregulated in the Sall4; Plzf double knockout hindlimb bud. In contrast, PLZF expression is reduced but detectable in Sall4; Gli3 double knockout limb buds, and SALL4 is expressed in the Plzf; Gli3 double knockout limb buds. These results indicate that Plzf, Gli3, and Hox10 genes downstream of Sall4, regulate femur and tibia development. In the autopod, we show that Sall4 negatively regulates Hedgehog signaling, which allows for development of the most anterior digit. Collectively, our study illustrates genetic systems that regulate development of the proximal-anterior skeletal elements in hindlimbs.