anti-Scleraxis Homolog A (Mouse) (SCXA) Antikörper

Mouse (Murine) Scleraxis Homolog A (Mouse) (SCXA) Interaktionspartner

1. The absence of Scx results in a defect in progenitor differentiation into Scx-expressing tenocytes and tendon repair.

2. These results highlighted the functional importance of both transient and persistent expression domains of Scx for proper integration of the musculoskeletal components.

3. Deletion of Scx led to altered long bone properties and callus healing.

4. scleraxis was required for TGFbeta-induced fibronectin expression: TGFbeta lost its ability to induce fibronectin expression following scleraxis knockdown.

5. The phosphorylation sequence matched that targeted by Casein Kinase 2, and inhibition of this kinase activity disrupted the ability of scleraxis to modulate the expression of its target genes while also attenuating TGFbeta-induced expression of type I collagen and myofibroblast phenotype conversion marker genes

6. Cardiac fibroblast phenotype regulation by scleraxis.

7. deletion of Scx led to impairments in enthesis structure.

8. several mRNAs are affected by alternative splicing events in the absence of Scx, suggesting additional roles in post-transcriptional modification.

9. Expression and function of scleraxis in the developing auditory system.

10. These studies identify an important role for Scx in regulating proteoglycans in embryonic and mature valve cells.

11. paratenon cells, which normally do not express Scx, respond to injury by turning on Scx and assembling matrix to bridge the defect

12. Smad3 binds Scleraxis and Mohawk and regulates tendon matrix organization.

13. Findings suggest a modular model for bone development, involving a distinct pool of Sox9- and Scx-positive progenitor cells that form bone eminences under regulation of TGFbeta and BMP4 signaling

14. the Scx(+)/Sox9(+) progenitor pool is a unique multipotent cell population that gives rise to tenocytes, ligamentocytes and chondrocytes for the establishment of the chondro-tendinous/ligamentous junction

15. Scx and Id1 are involved in the BMP4-Smad1-SMA signal transduction pathway besides the TGFbeta1-Smad1-SMA signaling pathway and modulate phenotypic changes in MCs in diabetic nephropathy.

16. Two proepicardial markers (Scleraxis and Semaphorin3D) were identified that genetically delineate heretofore uncharacterized proepicardial subcompartments.

17. Mechanical signaling exerts an important influence on the expression of genes, namely scleraxis (Scx) and type I collagen, which play a role in determining the tendon phenotype.

18. In addition to regulating the embryonic formation of limb tendons, scleraxis also appears to play an important role in the adaptation of adult tendons to physiological loading.

19. Transforming growth factor-beta induces skeletal muscle atrophy and fibrosis through the induction of atrogin-1 and scleraxis.

20. Scleraxis is required for differentiation of the stapedius and tensor tympani tendons of the middle ear.

Human Scleraxis Homolog A (Mouse) (SCXA) Interaktionspartner

1. Abnormal upregulation of HIF-2alpha served as a key switch to direct TSPCs differentiation into osteochondral-lineage rather than teno-lineage. Notably, Scleraxis (Scx), an essential tendon specific transcription factor, was suppressed on constitutive activation of HIF-2alpha and mediated the effect of HIF-2alpha on TSPCs fate decision.

2. These studies identify an important role for Scx in regulating proteoglycans in embryonic and mature valve cells.

3. Scleraxis was expressed in periodontal ligament cells, bone marrow cells, and gingival fibroblasts, and may play an important role in differentiation of periodontal ligament cells.

4. High glucose inhibited osteogenetic differentiation of periodontal ligament cells and up-regulated Scleraxis expression.

5. Scx and E47 might modulate the primary chondrogenesis by associating with the Sox9-related transcriptional complex, and by binding to the conserved E-box on Col2a1 promoter.

6. collagen type I and several T/L-related proteoglycans were upregulated in hMSC-Scx cells

7. Scleraxis thus appears to play a key role in the transcriptional regulation of type I collagen synthesis.