Aperçu des produits pour anti-SMAD, Mothers Against DPP Homolog 1 (SMAD1) Anticorps

Zebrafish SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. Data show that interplay of Smad1/5 and MAP kinase signaling system (ERK signalling) is essential for haemogenic endothelium-based haematopoietic stem cell emergence.

2. this study uncovers that smad1 and smad9 act redundantly to each other downstream of smad5 to mediate ventral specification and to regulate embryonic myelopoiesis.

3. that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 and Smad5.

Fruit Fly (Drosophila melanogaster) SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. this study shows transcriptional up-regulation of the TGF-beta intracellular signaling transducer Mad of Drosophila larvae in response to parasitic nematode infection

2. This report provides a genetic analysis of primary nociceptive neuron mechanisms that promote sensitization in response to injury. Drosophila melanogaster larvae whose primary nociceptive neurons were reduced in levels of specific components of the BMP signaling pathway, were injured and then tested for nocifensive responses to a normally subnoxious stimulus.

3. LTR sequence of the MDG4 retrotransposon contains the MAD protein binding site that affects the east-dependent repression

4. we identify key roles for the Zelda and Zerknullt transcription factors in establishing the resulting expression domain, and find widespread binding of insulator proteins to the Mad and Brinker-bound genomic regions. Analysis of embryos lacking the BEAF-32 insulator protein shows reduced transcription of a peak BMP target gene and a reduction in the number of amnioserosa cells, the fate specified by peak BMP signaling.

5. Mad linker phosphorylations control the intensity and range of the BMP-activity gradient in developing Drosophila tissues.

6. During development, synaptic pMad accumulation followed the arrival and clustering of ionotropic glutamate receptors at neuromuscular junction synapses.

7. The actions of Brat at synapses are mediated through mothers against decapentaplegic (Mad), the signal transduction effector of the bone morphogenetic protein (BMP) signaling pathway.

8. Data show that dSmad2 directly influences Baboon's phosphorylation of Mad.

9. Wg signaling via Zw3 and mad restricts self-renewal of sensory organ precursor cells

10. Mad has distinct signal transduction roles in the BMP and Wnt pathways depending on its phosphorylation state.

11. Nup154 controls nuclear localization of Mad transcription factor, but does not interact directly with it.

12. Yorkie and Mad physically bind each other, and 410 bp minimal enhancer of bantam that responds to Yorkie:Mad in vivo and in cultured cells, was identified.

13. Heterodimers of SAX and TKV play an important role in extending the BMP activity gradient by facilitating DPP diffusion and assisting GBB signaling through functional complexes with type II receptors.

14. importin-beta11 function interacts with the bone morphogenic protein pathway to regulate a pool of phosphorylated mothers against decapentaplegic that must be present at the presynapse for its proper development and function

15. Mad depletion or overexpression produced Wingless-like embryonic segmentation phenotypes

16. The downstream transcription factor Mothers against dpp is essential for the normal structural and functional development of the Drosophila neuromuscular junction, a synapse that displays activity-dependent plasticity.

17. dSmurf specifically targets phosphorylated MAD to proteasome-dependent degradation and regulates DPP signaling during development.

18. compared patterns of two related cellular responses, both signal-dependent phosphorylation of the BMP-regulated R-SMAD, MAD, and signal-dependent changes in levels and sub-cellular distribution of the co-SMAD Medea

19. the trimeric Mad-Medea complex binds Dpp-responsive silencers

20. a complex of the homologous Drosophila Smad proteins, Mad and Medea, is capable of concerted binding to GC-rich and SBE sites separated by as much as 20 bp.

Human SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. Here, the authors show that TGF-beta-induced SMAD1/5 phosphorylation requires members of two classes of type I receptor, TGFBR1 and ACVR1, and establish a new paradigm for receptor activation where TGFBR1 phosphorylates and activates ACVR1, which phosphorylates SMAD1/5.

2. analysis of the structural basis for R-SMAD recognition by MAN1 using SMAD2-MAN1 and SMAD1-MAN1 complex structures

3. miR-23a facilitated cell proliferation and migration by targeting BMPR2/Smad1 signaling in hypoxia-induced human pulmonary artery smooth muscle cells.

4. the expression of BMP15 in follicular fluid and Smad1 in granulosa cells was significantly decreased in the PCOS group compared with the control (P<0.05). The data suggested that the BMP15/Smad1 signalling pathway may be involved in granulosa cell apoptosis

5. Mechanical stress affects the osteogenic differentiation of human ligamentum flavum cells via the BMP-Smad1 signaling pathway.

6. Urinary Smad1 was associated with the degree of mesangial expansion in early diabetic nephropathy.

7. Differential expression of TGF-beta superfamily members and role of Smad1/5/9-signalling in chondral versus endochondral chondrocyte differentiation.

8. Uev1A appears to be involved in the BMP signaling pathway in which it collaborates with a ubiquitin E3 ligase Smurf1 to promote Smad1 degradation in a Ubc13-independent manner.

9. Data show that miR-26b-5p suppresses Twist1-induced EMT, invasion, and metastasis of HCC cells by targeting SMAD1.

10. Testosterone promoted tube formation of human umbilical endothelial cells, which was blocked by c-Src and ERK1/2 inhibitors or by the knockdown of Smad1.

11. Low doses of IL1B activate the BMP/Smad signaling pathway to promote the osteogenesis of periodontal ligament stem cells, but higher doses of IL1B inhibit BMP/Smad signaling through the activation of NF-kappaB and MAPK signaling, inhibiting osteogenesis.

12. Store operated calcium entry negatively regulates the Smad1 signaling pathway and inhibits Col IV protein production in glomerular mesangial cells.

13. A significant association was found between the low expression of inhibitory protein SMAD-7 and both zeta-chain-associated protein kinase 70-negative cells (p = 0.04) and lower apoptotic index (p = 0.004). No differences were observed in SMAD-2/3 expression. In conclusion, our results demonstrate a significant correlation between greater SMAD-1/8 and lower SMAD-4 expression in chronic lymphocytic leukemia cells

14. melatonin treatment was found to downregulate TNFalpha-induced SMURF1 expression and then decrease SMURF1-mediated ubiquitination and degradation of SMAD1 protein

15. The expression of specific targets Smad1 and Osterix was significantly increased in the presence of Pi and restored by coincubation with Mg(2+). As miR-30b, miR-133a, and miR-143 are negatively regulated by Pi and restored by Mg(2+) with a congruent modulation of their known targets Runx2, Smad1, and Osterix, our results provide a potential mechanistic explanation of the observed upregulation of these master switches of o

16. the BMP-2/Smad1/5/RUNX2 signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin synth

17. Regulation of impaired angiogenesis in diabetic dermal wound healing by microRNA-26a is mediated by the increased expression of its target gene, SMAD1.

18. The expression SMAD1 protein showed a significant correlation with lung cancer differentiation and lymphatic metastasis (P < 0.05), but not with genders, ages, tumor sizes and histological types of lung cancer patients (P>0.05).

19. Overexpression of Smad1 is associated with prostate cancer.

20. SMAD1 signaling may be a key pathway contributing the pathogenesis of Cardio-facio-cutaneous syndrome during early development.

Mouse (Murine) SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. NEDD4 enhances osteoblast proliferation by removing pSMAD1 activated by TGFbeta1.

2. SMAD1/5 signaling in osteoclasts regulates bone formation via coupling factors.

3. TGF-beta/Smad proteins signaling affects radiation response and prolongs survival by regulating DNA repair genes in malignant glioma.

4. the reduced bone formation in GIO mice could not only be prevented by osteoblasts-specific Ckip-1 ablation, but also be attenuated after osteoblasts-specific Smad1 overexpression

5. Results show that Smad1 plays an important role in the development of glomerular injury without affecting cell proliferation, in progressive glomerulonephritis.

6. These findings uncover crosstalk between the BMP-Smad1 and RANKL-NF-kappaB pathways during osteoclastogenesis that underlies the action of active vitamin D on bone health.

7. CD137 signaling is a new regulator of angiogenesis by modulating the Smad1/5-NFATc1 pathway.

8. TGF-beta1-induced pSmad1 levels were elevated in Nedd4-deficient primary VSMCs isolated from Nedd4(fl/fl) ;SM22alpha-Cre mice.

9. AA-enhanced cardiomyogenesis thus relies on the ability of AA to modulate the ratio of SMAD signaling among the TGFbeta-superfamily receptor signaling pathways

10. Sphingosine 1 phosphate also up-regulated runt-related transcription factor 2 (Runx2) expression through S1PR2/RhoA/ROCK/Smad1/5/8 signaling.

11. these results identify the PI3K-GSK3-SMAD1 axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.

12. We discovered that Smad1/5/4-Amhr2-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1/5/4-Amhr2-cre KO females exhibit multiple defects in stroma, epithelium, and smooth muscle layers and fail to assemble a closed uterine lumen upon embryo implantation, with defective uterine decidualization that led to pregnancy loss at early to mid-gestation.

13. these studies characterize an accessory TGF-beta-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung.

14. these results identify a novel function of YAP in neocortical astrocytic differentiation and proliferation, and reveal a BMP2-YAP-SMAD1 pathway underlying astrocytic differentiation in the developing mouse neocortex.

15. Dynamin-dependent endocytosis of Bone Morphogenetic Protein2 (BMP2) and its receptors is dispensable for the initiation of Smad signaling

16. Thyroid-specific Smad1 and Smad5 double-knockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular architecture.

17. Smad1 and Smad5 have overlapping functions to govern hepcidin transcription. Moreover, erythropoietin and erythroferrone target Smad1/5 signaling and require Smad1/5 to suppress hepcidin expression.

18. Actin cytoskeleton depolymerization inhibites BMP2 signaling via blocking of Smad by dephosphorylated CNN1 in osteoblast cells under simulated microgravity.

19. Store operated calcium entry negatively regulates the Smad1 signaling pathway and inhibits Col IV protein production in glomerular mesangial cells.

20. Thus, our findings identify an unrecognized function of neogenin in mouse neocortical astrocyte differentiation, and suggest a signaling pathway, BMP2-neogenin-YAP-Smad1, underlying astrogliogenesis in developing mouse neocortex.

Xenopus laevis SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. interactions between miR-26 and the Smad1 3'UTR modulate Smad1 function in the establishment of axial patterning.

Cow (Bovine) SMAD, Mothers Against DPP Homolog 1 (SMAD1) interaction partners

1. a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.