Browse our anti-ADAM17 (ADAM17) Antibodies

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

1. 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.

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

3. 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)

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

5. 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

6. 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.

7. Conditional ADAM17 knockout mice lacking ADAM17 in all leukocytes had a significant survival advantage during severe polymicrobial sepsis induced by CLP, associated with enhanced neutrophil recruitment at the infectious locus along with decreased bacterial spread and circulating levels of proinflammatory factors. Its induction during sepsis may tip the balance between efficient and impaired neutrophil recruitment.

8. These results demonstrate a novel physiologic role for a disintegrin and metalloprotease 17 in regulating murine IL-6 (show IL6 Antibodies) signals during inflammatory processes.

9. These results show that TACE is a target of, and is downregulated by, soluble TNF (show TNF Antibodies)-induced AP-2alpha (show TFAP2A Antibodies) transcription factor in dendritic cells

10. the critical role of the transmembrane domains of ADAM17 and Rhbdf2 (show RHBDF2 Antibodies) in the regulation of the ADAM17 and EGFR (show EGFR Antibodies), and ADAM17 and TNFalpha (show TNF Antibodies) signaling pathways, was examined.

Human ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. 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.

2. 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.

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

4. ADAM17 may be a key enzyme that regulates the generation of TNF-alpha (show TNF Antibodies) in oral keratinocytes.

5. therapies against ADAM10 (show ADAM10 Antibodies) and ADAM17 may promote cancer stem cell migration away from the tumourigenic niche resulting in a differentiated phenotype that is more susceptible to treatment.

6. ADAM10 (show ADAM10 Antibodies) and ADAM17 are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes.For ADAM17 phosphatidylserine exposure is required to then induce its shedding function.

7. In the present study, the authors show that deletion of a triple serine (3S) motif (Ser (show SIGLEC1 Antibodies)-359 to Ser (show SIGLEC1 Antibodies)-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17, but not ADAM10 (show ADAM10 Antibodies). We find that the impaired shedding is caused by the reduced distance between the cleavage site and the plasma membrane.

8. ADAM17 is a Western diet-inducible enzyme activated by CXCL12 (show CXCL12 Antibodies)-CXCR4 (show CXCR4 Antibodies) signaling, suggesting the pathway: Western diet-->CXCL12 (show CXCL12 Antibodies)-->CXCR4 (show CXCR4 Antibodies)-->ADAM17-->TGFalpha-->EGFR (show EGFR Antibodies). ADAM17 might serve as a druggable target in chemoprevention strategies

9. The regulation of the shedding activity of ADAM17 is multilayered and different regions of the protease are involved. Intriguingly, its extracellular domains play crucial roles in different regulatory mechanisms. We will discuss the role of these domains in the control of ADAM17 activity.

10. We show ADAM17 expression in human dopaminergic neurons derived from induced pluripotent stem cells and we discuss how this state-of-the-art technology can be further exploited to study the function of this important protease in the brain and other tissues.

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