Browse our anti-ADAM17 (ADAM17) Antibodies

Mouse (Murine) ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. results suggest ADAM17/EGFR-driven PLCgamma1 and PKC pathways as important promoters of TG1 expression during terminal keratinocyte differentiation.

2. iRhom2 (show RHBDF2 Antibodies) controls multiple aspects of TACE biology, including stimulated shedding on the cell surface.

3. Targeting ADAM17 with a lentiviral vector attenuates endotoxemia in mice.

4. Addition of a disintegrin and metallopeptidase domain 17 (ADAM17) to the culture supernatant of stimulated splenocytes decreased Interferon-gamma (IFN-gamma (show IFNG Antibodies)) concentration.

5. Overall, iRhom2 (show RHBDF2 Antibodies) binds to TACE throughout its lifecycle, implying that iRhom2 (show RHBDF2 Antibodies) is a primary regulator of stimulated cytokine and growth factor signalling.

6. Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR (show EGFR Antibodies)-ligands by differentially activating ADAM17 or ADAM10 (show ADAM10 Antibodies).

7. Fhl2 (show FHL2 Antibodies) anticipates the emerging inflammation and specifically the development of psoriatic arthritis by impeding the Adam17-mediated release of TNF (show TNF Antibodies)

8. most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR (show EGFR Antibodies)

9. ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms

10. In a clinically relevant CADASIL (show NOTCH3 Antibodies) mouse model, we show that exogenous ADAM17 or HB-EGF (show HBEGF Antibodies) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Antibodies) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 Antibodies)-induced deficits.

Human ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. ADAM-17 in inflammatory myopathy was significantly higher than that in healthy control. ADAM-17 in post-treatment with corticosteroid and/or immunosuppressant serum was significantly decreased compared with that in pre-treatment serum.

2. The present research suggests that ADAM17shRNA can inhibit MCF7 cell invasion and proliferation in vitro and inhibit MCF7 xenograft growth in vivo through the EGFR (show EGFR Antibodies)/PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) and EGFR (show EGFR Antibodies)/MEK (show MAP2K1 Antibodies)/ERK (show EPHB2 Antibodies) signaling pathways.

3. Uev1A (show UBE2V1 Antibodies)-Ubc13 (show UBE2N Antibodies) complex catalyzes lysine63-linked ubiquitination of RHBDF2 (show RHBDF2 Antibodies) to promote TACE maturation.

4. ADAM17 plays a role in chronic kidney disease-mineral and bone disorder.

5. Insulin-like growth factor-1 (show IGF1 Antibodies) activates different catalytic subunits p110 (show CUX1 Antibodies) of PI3K (show PIK3CA Antibodies) in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 (show ADAM10 Antibodies) and ADAM17.

6. ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 (show TREM2 Antibodies) after Histidine 157. Findings reveal a link between shedding of TREM2 (show TREM2 Antibodies) and its regulation during inflammatory conditions or chronic neurodegenerative disease in which activity or expression of sheddases might be altered.

7. Oxidative stress is correlated with hyperactivation of the ADAM17/Notch (show NOTCH1 Antibodies) signaling pathway and a consequent increase in fibrosis in patients with endometriosis.

8. Plasma levels of ADAM17 are increased in Tanzanian children hospitalized with a malaria infection compared with asymptomatic children but similar to children hospitalized with other infectious diseases. The plasma levels of ADAM17 decreased during recovery after an acute malaria episode.

9. Data found that ADAM17 is constitutively internalized by clathrin-coated pits and that physiological stimulators such as GPCR (show NMUR1 Antibodies) ligands induce ADAM17-mediated shedding, but do not alter the cell-surface abundance of the protease. Also, physiological activation of ADAM17 does not rely on its relocalisation, but that PMA-induced PKC (show PRRT2 Antibodies) activity drastically dysregulates the localisation of ADAM17.

10. Cullin 3 (show CUL3 Antibodies) regulates ADAM17-mediated ectodomain shedding of AREG (show AREG Antibodies).

Pig (Porcine) ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. these findings provide the direct evidence that ADAM17 cleaves porcine TNFalpha (show TNF Antibodies), which represents a new view for identifying potential therapeutic targets in anti-porcine reproductive and respiratory syndrome virus therapy

2. ADAM17 was involved in porcine CD16 (show CD16 Antibodies) shedding in porcine reproductive and respiratory syndrome virus-infected pigs.

3. Overexpression of ADAM17 induced downregulation of CD163 (show CD163 Antibodies) expression and a reduction in reproductive and respiratory syndrome virus infection.

4. activation of TACE/ADAM17 via a PKC (show FYN Antibodies)-induced c-Src (show SRC Antibodies)-dependent manner mediates proteolytic activation of the EGF (show EGF Antibodies)-like factors that are involved in the induction of granulosa cell differentiation, cumulus expansion, and meiotic maturation of porcine oocytes

5. Data indicate that TNF-alpha (show TNF Antibodies) stimulates Rac (show AKT1 Antibodies), ADAM17/TACE, and RhoA (show RHOA Antibodies) through the guanine nucleotide exchange factor (show ARHGEF12 Antibodies) (GEF)-H1 (show ARHGEF2 Antibodies).

6. progesterone-induced TACE/ADAM17 leads to production of soluble EGF (show EGF Antibodies) domain from cumulus cells, which enhances functional changes of cumulus cells and progresses meiotic maturation of oocytes