Growth Arrest-Specific 1 (GAS1) ELISA Kits

Human Growth Arrest-Specific 1 (GAS1) interaction partners

1. Studies establish Gas1 as a negative regulator in colorectal cancer.

2. These results demonstrated that miR-184 and the GAS1/Akt pathway may be a potential therapeutic target for intervertebral disc degeneration.

3. WT1 modulates Akt/JNK signaling pathway mediated autophagy by controlling the expression of growth arrest-specific 1 (Gas1).

4. Downregulation of GAS1 is associated with clear cell renal cell carcinoma.

5. the synergistic effect of Gas1 inhibition and GDNF against glutamate-induced cell injury in human SH-SY5Y neuroblastoma cells, is reported.

6. solutions structure and biophysical characterization of the multifaceted signalling effector protein growth arrest specific-1

7. This review summarizes the structure of Gas1 and molecular mechanism of action during embryonic development and cellular functions.

8. GAS1 is a novel endogenous inhibitor of glomerular mesangial cell proliferation.

9. Growth arrest-specific gene 1 is downregulated and inhibits tumor growth in gastric cancer.

10. GAS1 induced the activity of caspase-3 and resulting in apoptosis of the cells.

11. Interference of endoplasmic reticulum to Golgi transport increased immature amyloid beta protein precursor accumulation upon Gas1 expression in lipid raft fractions.

12. we demonstrate that sequence variants in GAS1 can impair its physical interaction with SHH, suggesting a decrease in the SHH downstream signaling cascade as a pathogenic mechanism of disease.

13. Gas1 is a novel APP-interacting protein involved in the control of APP maturation and processing.

14. Growth arrest-specific gene 1 contributes to predicting metastasis or recurrence in stage II and III colorectal cancer.

15. GAS1 could be considered a candidate locus for one of the types of human holoprosencephaly.

16. Gas1 is related to the GDNF alpha receptors and regulates Ret signaling

17. This review considers the possible involvement of GAS1 in genetic diseases, stem cell renewal, and cancer growth through its cooperative activity with Hedgehog (HH) growth factor and the HH receptor.

18. Gas1 is a molecule involved in cell arrest that can induce apoptosis when over-expressed in different cell lines.

19. Gas1 has all the expected properties of a melanoma tumor suppressor: suppression of metastasis in a spontaneous metastasis assay, promotion of apoptosis following dissemination of cells to secondary sites, and down-regulation in human melanoma metastasis.

20. Results present evidence demonstrating that Gas1 exerts its effects inhibiting cell growth and inducing apoptosis of glioma cells in the absence of Shh.

Mouse (Murine) Growth Arrest-Specific 1 (GAS1) interaction partners

1. that Gas1 is a direct target of NeuroD1 during the induction of the neurogenic program

2. Gas1 is expressed and released by neurons and promotes differentiation

3. Western blot and immunofluorescence analyses showed two GIP-anchored proteins were clearly involved in the fertilisation process, namely growth arrest specific 1 (Gas1) and glial cell line-derived neurotrophic factor receptor alpha1 (Gfralpha1). This was demonstrated by evaluating oocyte fertilisability after treatment of oocytes with antibodies against the selected proteins, with their respective short interference RN...

4. Findings provide evidence for a dual requirement for Boc and Gas1 during early development of the palate, mediating cell cycle regulation during growth and subsequent fusion of the palatal shelves.

5. The results suggest that in diabetes the decrease of Gas1 promotes the activation of parietal progenitor cells of Bowman's capsule that might differentiate into podocytes and compensate their loss observed in this pathology.

6. Up-regulation of inducible Gas1 contributed to the apoptosis of reactive astrocytes in injured substantia nigra.

7. The C/EBP target Gas1 is induced in granulosa cells and is associated with ovulation and luteinization.

8. the overexpression of Gas1 (growth arrest specific 1) gene reduces the size, proliferating activity and malignancy of liver tumors.

9. WT1 modulates receptor tyrosine kinase signaling in nephron progenitor cell by directing the expression of Gas1.

10. When Shh is presented as a point source, enteric axons turn away from it in a Gas1-dependent manner.

11. We demonstrated that tGas1 has an antineoplastic effect, and the results support the potential of tGas1 as an adjuvant for the treatment of gliomas

12. widespread distribution and cellular localization of the GAS1 native protein in adult mammalian CNS

13. finding that Gas1 is transcribed at the G(1)/S transition suggests that the gene may exert a novel function during cell proliferation.

14. Gas1 promotes myogenic differentiation through regulation of cell cycle arrest and is critical to activate p38MAPK

15. Genetic loss-of-function of GAS1, CDO, and BOC in SHH is associated with defective neural patterning.

16. Gas1 acts to maintain high levels of FGF10 at the tip mesenchyme and support the proposal that Fgf10 expression in this region is crucial for maintaining Fgf8 expression in the AER

17. Gas1 is related to the GDNF alpha receptors and regulates Ret signaling

18. GAS1 acts cooperatively with Patched1 for Hedgehog binding and enhances signaling activity in a cell-autonomous manner.

19. Gas1 and Cdo cooperate to promote Shh signaling during neural tube patterning, craniofacial, and vertebral development

20. Loss of a single Shh allele in a Gas1(-/-) background significantly exacerbated the midline craniofacial phenotype, providing genetic evidence that Shh and Gas1 interact.