Tissue inhibitor of metalloproteinase-3 (TIMP-3) is a dual inhibitor of the matrix metalloproteinases (MMPs) and some adamalysins, two families of extracellular and cell surface metalloproteinases that function in extracellular matrix turnover and the shedding of cell surface proteins. The mechanism of inhibition of MMPs by TIMPs has been well characterized, and since the catalytic domains of MMPs and adamalysins are homologous, it was assumed that the interaction of TIMP-3 with adamalysins is closely similar. Here we report that the inhibition of the extracellular region of ADAM-17 (tumor necrosis factor alpha-converting enzyme (TACE)) by the inhibitory domain of TIMP-3 (N-TIMP-3) shows positive cooperativity. Also, mutations in the core of the MMP interaction surface of N-TIMP-3 dramatically reduce the binding affinity for MMPs but have little effect on the inhibitory activity for TACE. These results suggest that the mechanism of inhibition of ADAM-17 by TIMP-3 may be distinct from that for MMPs. The
TY - JOUR. T1 - The disintegrin-like metalloproteinase ADAM 10 is involved in coinstitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion. AU - Hundhausen, C.. AU - Misztela, D.. AU - Berkhout, Theo. AU - Broadway, N.. AU - Saftig, P.. AU - Reiss, K.. AU - Hartmann, D.. AU - Fahrenholz, F.. AU - Postina, R.. AU - Matthews, J.. AU - Kallen, K.J.. AU - Rose-John, S.. AU - Ludwig, A.. PY - 2003/8/15. Y1 - 2003/8/15. N2 - The CX3C chemokine fractalkine (CX3CL1) exists as a membrane-expressed protein promoting cell-cell adhesion and as a soluble molecule inducing chemotaxis. Transmembrane CX3CL1 is converted into its soluble form by defined proteolytic cleavage (shedding), which can be enhanced by stimulation withphorbol-12-myristate-13-acetate (PMA). PMA-induced CX3CL1 shedding has been shown to involve the tumor necrosis factor-alpha-converting enzyme (TACE), whereas the constitutive cleavage in unstimulated cells remains elusive. Here we demonstrate a role of ...
Adam protein (A Disintegrin and Metalloproteinase Protein) is a family of peptidase proteins[1]. ADAMs are also known as the Adamalysin family. ADAMs are classified as Sheddases because they cut off or shed extracellular portions of transmembrane proteins. For example, ADAM 10 can cut off part of the HER2 receptor, activating it[2] and ADAM 17 can cut off part of the EGFR once it has bound its ligand, freeing the ligand to go and stimulate another cell[3]. Therapeutic ADAM inhibitors can potentiate anti-cancer therapy[citation needed]. It is categorized under EC 3.4.24.46. Types include: ...
in Molecular Medicine (2006), 12(7-8, Jul-Aug), 171-179. ADAMs (a disintegrin and metalloprotease) constitute a family of cell surface proteins containing disintegrin and metalloprotease domains which associate features of adhesion molecules and proteases ... [more ▼]. ADAMs (a disintegrin and metalloprotease) constitute a family of cell surface proteins containing disintegrin and metalloprotease domains which associate features of adhesion molecules and proteases. ADAMTSs (a disintegrin and metalloprotease with thrombospondin motifs) bear thrombospondin type I motifs in C-terminal extremity, and most of them are secreted proteins. Because genetic studies have shown that ADAM-33 gene polymorphisms are associated with asthma, we designed this study to assess mRNA expression profile of several ADAM and ADAMTS proteases in sputum from patients with asthma and to investigate the relationship between expression of these proteases and asthma-associated inflammation and airway obstruction. mRNA ...
TY - JOUR. T1 - A computational model of the LGI1 protein suggests a common binding site for ADAM proteins. AU - Leonardi, Emanuela. AU - Andreazza, Simonetta. AU - Vanin, Stefano. AU - Busolin, Giorgia. AU - Nobile, Carlo. AU - Tosatto, Silvio C E. PY - 2011/3/29. Y1 - 2011/3/29. N2 - Mutations of human leucine-rich glioma inactivated (LGI1) gene encoding the epitempin protein cause autosomal dominant temporal lateral epilepsy (ADTLE), a rare familial partial epileptic syndrome. The LGI1 gene seems to have a role on the transmission of neuronal messages but the exact molecular mechanism remains unclear. In contrast to other genes involved in epileptic disorders, epitempin shows no homology with known ion channel genes but contains two domains, composed of repeated structural units, known to mediate protein-protein interactions. A three dimensional in silico model of the two epitempin domains was built to predict the structure-function relationship and propose a functional model integrating ...
Disintegrin-like metalloproteases (ADAMs) comprise the major family of ectodomain sheddases. In inflammatory settings, ADAMs mediate signaling of cytokines, including TNFα and IL-6, and control leukocyte recruitment by the cleavage of cell adhesion molecules. ADAM17 and ADAM10 have been implicated in diverse diseases associated with inflammation, including psoriasis, asthma, arthritis, atherosclerosis, inflammation associated tumors, diabetes and Alzheimers disease (AD) [1-3]. With regard to the latter, it is assumed that decreased α-secretase (ADAM10 and ADAM17) activity and increased β-secretase (BACE1) activity results in abnormal processing of the amyloid precursor protein (APP). This leads to elevated levels of neurotoxic amyloid β, a key pathognomonic feature of AD. Due to the important role of ADAMs and BACE in amyloid β production, altering the ADAM10/17 and/or BACE function are being considered as a promising therapeutic approach to AD [4].. Although ADAM10 and ADAM17 were ...
Abstract. The transmembrane protein ADAM22 is expressed at high levels in the brain. From its molecular structure, ADAM22 is thought to be an adhesion molecule or a receptor because it has functional disintegrin-like and cysteine-rich sequences in its ectodomain. The phenotypic analysis of ADAM22-deficient mice has indicated the important roles played by ADAM22 in proper neuronal function and peripheral nerve development, however, the precise molecular function of ADAM22 is still unknown. To understand the function of ADAM22 on a molecular basis, we identified ADAM22 binding proteins by using immunoprecipitation and mass spectrometric analysis. This analysis revealed that Leucine-rich glioma inactivated 1 (LGI1) is the most potent ADAM22 binding protein in mouse brain. By our quantitative cell-ELISA system, we demonstrated the specific binding of LGI1 with ADAM22. Furthermore, we showed that LGI4, a putative ADAM22 ligand, also bound to ADAM22. Characterization of the binding specificity of LGI1 ...
ADAM (a disintegrin and metalloproteinase) 10 is a key member of the ADAM family of disintegrin and metalloproteinases which process membrane-associated proteins to soluble forms in a process known as shedding. Among the major targets of ADAM10 are Notch, EphrinA2 and CD44. In many cell-based studies of shedding, the activity of ADAM10 appears to overlap with that of ADAM17, which has a similar active-site topology relative to the other proteolytically active ADAMs. The tissue inhibitors of metalloproteinases, TIMPs, have proved useful in the study of ADAM function, since TIMP-1 inhibits ADAM10, but not ADAM17; however, both enzymes are inhibited by TIMP-3. In the present study, we show that, in comparison with ADAM17 and the MMPs (matrix metalloproteinases), the N-terminal domains of TIMPs alone are insufficient for the inhibition of ADAM10. This knowledge could form the basis for the design of directed inhibitors against different metalloproteinases.. ...
specificalIntended Uses: This ADAM10 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human ADAM10. This ELISA kit for research use only, not for therapeutic or diagnostic applications! Principle of the Assay,,ADAM10 ELISA kit applies the competitive enzyme immunoassay technique utilizing a polyclonal anti-ADAM10 antibody and an ADAM10-HRP conjugate. The assay sample and buffer are incubated together with ADAM10-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the ADAM10 concentration since ADAM10 from ...
The Adam and Dr. Drew Show. Guest - The Love Between The Two Hosts. Recorded 07-28-2015 - Release Date 07-30-2015. Production Number #259 - The Syndrome. Show Page. Adam opens the show with the standard intro, Drew says hes trying to recover from being yelled at, Adam addresses "The Syndrome" at play, the same think Dr. Bruce has but in a milder form.. Adam is now continuing his argument about ID and what Dr. Drew uses for airport security.. Adam is breaking down Dr. Bruces syndrome and how he doesnt know hes alive unless Adam is yelling at him.. Adam says that Bruce needs to be yelled at, like a battered woman seeking to recreate the trauma of her past, Drew is connecting this to Bruce and his family of origin.. Drew says Adam needs to yell while these people need him to yell at them, Adam says he doesnt yell at Mark Geragos and says you can measure his yelling by the order of biggest fuck ups.. Adam talks about what a klutz does or doesnt do, Adam is talking about shedding foam rubber ...
Exclusive to Global Medical Discovery (new Significance Statement and new figure). The role of metalloproteinase ADAM17 in regulating
Many guidance receptors are proteolytically cleaved by membrane-associated metalloproteases of the ADAM family, leading to the shedding of their ectodomains. Ectodomain shedding is crucial for receptor signaling and function, but how this process is controlled in neurons remains poorly understood. Here, we show that the transmembrane protein Lrig2 negatively regulates ... read more ADAM-mediated guidance receptor proteolysis in neurons. Lrig2 binds Neogenin, a receptor for repulsive guidance molecules (RGMs), and prevents premature Neogenin shedding by ADAM17 (TACE). RGMa reduces Lrig2-Neogenin interactions, providing ADAM17 access to Neogenin and allowing this protease to induce ectodomain shedding. Regulation of ADAM17-mediated Neogenin cleavage by Lrig2 is required for neurite growth inhibition by RGMa in vitro and for cortical neuron migration in vivo. Furthermore, knockdown of Lrig2 significantly improves CNS axon regeneration. Together, our data identify a unique ligand-gated mechanism to ...
Purified Recombinant Human ADAM33 293 Cell Lysate from Creative Biomart. Recombinant Human ADAM33 293 Cell Lysate can be used for research.
Results-Treatment with recombinant ADAMTS 13 (rADAMTS 13) reduced the levels of chemokines and cytokines, myeloperoxidase activity, and microglia activation and neutrophil recruitment after ICH. rADAMTS 13 also decreased interleukin-6 expression in brain endothelial cells stimulated by lipopolysaccharide, whereas recombinant von Willebrand factor reversed this effect. The anti-inflammatory effect of rADAMTS 13 was accompanied by reduced expression of intercellular adhesion molecule-1 and less activation of matrix metalloproteinase, enhanced pericyte coverage of brain microvessels, and attenuated BBB disruption. Furthermore, neutrophil depletion protected against BBB damage, and rADAMTS 13 treatment had no further beneficial effect. Finally, treatment of mice with rADAMTS 13 reduced cerebral edema and hemorrhagic lesion volume and improved neurological functions. ...
ADAMs (a disintegrin and metalloproteinase) have important roles in development and diseases such as cancer. Previously, an ADAM15 splice variant (ADAM15B), which contains an inserted cytoplasmic Src-binding site, was linked to clinical aggressiveness in breast cancer, yet little was known about how this splice variant affects the function of ADAM15. Here, we show that ADAM15B has enhanced catalytic activity in cell-based assays compared with ADAM15A, which lacks a Src-binding site, using shedding of fibroblast growth factor receptor 2iiib variant as an assay for catalytic activity. Moreover, the enhanced activity of ADAM15B compared with ADAM15A depends on Src because it is abolished by Src-kinase inhibitors and in Src(-/-) cells, but not in Src(-/-) cells rescued with Src. These findings provide insights into the mechanism of how a splice variant linked to clinical agressiveness in breast cancer causes increased activity of ADAM15B, and suggest that inhibitors of the ADAM15 protease activity or of the
ADAMTS-20 is a 1,906 amino acid protein of the large family of secreted zinc-dependent metalloproteases known as the ADAMTS (a disintegrin and metalloprotease domain, with thrombospondin type-1 repeats) family (Figure 3). ADAMTS-20 has an N-terminal signal peptide and a propeptide domain which contains three conserved Cys residues and ends in a basic region (aa 246-259). Following the prodomain, ADAMTS-20 contains the zinc-coordinating catalytic sequence HELGHVFNVPHD (aa 399-410) that is closely related to sequences found in metalloproteases. The catalytic domain of ADAMTS-20 is followed by a disintegrin-like domain similar in size and structure amongst all ADAMTS proteins (76 residues) and includes eight conserved Cys residues. The disintegrin domain precedes a single thrombospondin type I repeat (TSP1) which is well-conserved and similar to a domain in Thrombospondin I. The first TSP1 repeat is followed by a cysteine (Cys)-rich domain that has ten conserved Cys residues as well as a spacer ...
A disintegrin and metalloprotease (ADAM) 10 and ADAM17 are ubiquitous transmembrane "molecular scissors" which proteolytically cleave, or shed, the extracellular regions of other transmembrane proteins. ADAM10 is essential for development because it cleaves Notch proteins to induce Notch signaling and regulate cell fate decisions. ADAM17 is regarded as a first line of defense against injury and infection, by releasing tumor necrosis factor α (TNFα) to promote inflammation and epidermal growth factor (EGF) receptor ligands to maintain epidermal barrier function. However, the regulation of ADAM10 and ADAM17 trafficking and activation are not fully understood. This review will describe how the TspanC8 subgroup of tetraspanins (Tspan5, 10, 14, 15, 17, and 33) and the iRhom subgroup of protease-inactive rhomboids (iRhom1 and 2) have emerged as important regulators of ADAM10 and ADAM17, respectively. In particular, they are required for the enzymatic maturation and trafficking to the cell surface of ...
BIOZYME, INC. BioZyme, Inc. is the only company to offer both selective and sensitive fluorescence substrates (FRET) for the Matrix Metalloproteinase (MMP) and A Disintegrin and Metalloproteinase (ADAM) Family members. We also have the most competitive pricing for fluorescence substrates (FRET) for the Matrix Metalloproteinase (MMP) and A Disintegrin and Metalloproteinase (ADAM) Family members as well as recombinant human ADAM8 enzyme.. See our online catalog or our individual Product Sheets located on this website.. Many of Biozyme, Inc. ADAM and MMP fluorescent substrates have been used successfully to screen biological samples of all kinds. All of our ADAM substrates and MMP substrates have been used in a technique called proteolytic matrix analysis or PrAMA to decipher the contributions of different metalloproteinase activities in a biological sample even though the substrates are not completely selective. With this technique, the MMP substrates and ADAM substrates have helped quantify MMP9, ...
Barreto-Luis A, Pino-Yanes M, Corrales A, Campo P, Callero A, Acosta-Herrera M, Cumplido J, Ma SF, Martinez-Tadeo J, Villar J, Garcia JG, Carrillo T, Carracedo Á, Blanca M, Flores C. Genome-wide association study in Spanish identifies ADAM metallopeptidase with thrombospondin type 1 motif, 9 (ADAMTS9), as a novel asthma susceptibility gene. J Allergy Clin Immunol. 2016 Mar; 137(3):964-6 ...
Allergic asthma severity may be associated with IgE levels. We have shown that beta-2 adrenergic receptor (β2AR) engagement on CD40L/IL-4-primed B cells increases the level of IgE produced per cell, without affecting class switch recombination. β2AR agonists alleviate bronchoconstriction by targeting the β2AR expressed on bronchiolar smooth muscle cells to trigger airway relaxation, but these drugs also target the β2AR on primed B cells, potentially producing an IgE effect that may be counterproductive to the drugs intended use. We reported that surface CD23 expression remained constant on primed B cells exposed to a β2AR agonist, while CD23 mRNA, total CD23 protein, and soluble CD23 (sCD23) increased. Thus, if sCD23 positively regulates IgE production, an increase due to β2AR engagement may worsen bronchoconstriction, albeit relieving it in the short term. We hypothesized that the primary sheddase of CD23, ADAM10, is regulated by β2AR engagement on a primed B cell. Although we found that ...
Protein ectodomain shedding is crucial for cell−cell interactions because it controls the bioavailability of soluble tumor necrosis factor-α (TNFα) and ligands of the epidermal growth factor (EGF) receptor, and the release of many other membrane proteins. Various stimuli can rapidly trigger ectodomain shedding, yet much remains to be learned about the identity of the enzymes that respond to these stimuli and the mechanisms underlying their activation. Here, we demonstrate that the membrane-anchored metalloproteinase ADAM17, but not ADAM10, is the sheddase that rapidly responds to the physiological signaling pathways stimulated by thrombin, EGF, lysophosphatidic acid and TNFα. Stimulation of ADAM17 is swift and quickly reversible, and does not depend on removal of its inhibitory pro-domain by pro-protein convertases, or on dissociation of an endogenous inhibitor, TIMP3. Moreover, activation of ADAM17 by physiological stimuli requires its transmembrane domain, but not its cytoplasmic domain, ...
FUNCTION: This gene encodes a member of a disintegrin and metalloprotease (ADAM) family of endoproteases that play important roles in various biological processes including cell signaling, adhesion and migration. This gene is specifically expressed in epididymis where the encoded protein is transferred to the sperm surface during epididymal transit. This gene is located adjacent to a related gene from the ADAM family of proteins on chromosome 14. [provided by RefSeq, Oct 2015 ...
The Adam and Dr. Drew Show. Guest - The Love Between the Two Hosts. Recorded 09-30-2014 - Release Date 10-09-2014. Production Number #181 - Sneaking Out of Bed in the Morning. Show Page. Adam and Drew open hour number 2 with some thanks for supporting the pirate ship, Adam plugs Mangria and explains the show will be Thursday only for the next few weeks, Drew once again thanks the guest hosts for filling in.. Drew asks Adam about his housewarming party, Drew missed it, he was out of town, Adam figured as much.. Adam is now telling everyone to do themselves a favor by throwing a party at their home and picking someone you care about from the airport once per year, youll get your shit in order, clean up your car, and clean the leaves off the roof and the skylights.. Adam is now waxing poetic on cleaning the landscape of your life, going in depth about the cleaning lengths he went to, including getting scuffs of the wall with the scratchy part of the sponge.. Adam has a conversation with Lynette ...
Animals have evolved multiple mechanisms to protect themselves from the cumulative effects of age-related cellular damage. Here, we reveal an unexpected link between the TNF (tumour necrosis factor) inflammatory pathway, triggered by the metalloprotease ADAM17/TACE, and a lipid droplet (LD)-mediated mechanism of protecting retinal cells from age-related degeneration. Loss of ADAM17, TNF and the TNF receptor Grindelwald in pigmented glial cells of the Drosophila retina leads to age-related degeneration of both glia and neurons, preceded by an abnormal accumulation of glial LDs. We show that the glial LDs initially buffer the cells against damage caused by glial and neuronally generated reactive oxygen species (ROS), but that in later life the LDs dissipate, leading to the release of toxic peroxidated lipids. Finally, we demonstrate the existence of a conserved pathway in human iPS-derived microglia-like cells, which are central players in neurodegeneration. Overall, we have discovered a pathway mediated
Human CellExp ADAM12, human recombinant protein, ADAM12, MCMP, MLTN, MLTNA, MCMPMltna, Meltrin Alpha validated in (PBV10869r-10), Abgent
NORTH ADAMS, Mass. - Dr. Leigh LoPresti has joined the primary care team at CHP North Adams Family Medical and Dental. A family medicine physician, LoPresti is a former chief medical...
Buy ADAM10 recombinant protein, A Disintegrin and Metalloproteinase Domain 10 Recombinant Protein-NP_001101.1 (MBS143712) product datasheet at MyBioSource, Recombinant Proteins
fertilin: fertilin is a sperm surface protein involved in sperm-egg fusion; consists of two subunits, fertilin alpha and beta, both of which belong to the metalloprotease-disintegrin protein family; RefSeq NM_172126 (Adam1a, mouse); NM_172125 (Adam1b, mouse); NM_009618 (Adam2, mouse); NM_020078 (Adam1a, rat); NM_020077 (Adam2, rat); NM_001464 (ADAM2, human)
No we are not inbred. On the fifth day God created the first Adams. They were many Adams or humans, who were infact able to procreate on their own it seems being completely God like. All until the Adam of YHWH couldnt find anyone he could love. No matter who he would choose among those perfect creatures of God, he could never feel that he owned it, or that she could be the part of him that he missed. He had it all, he didnt need anything the other Adams had. Then YHWH let a deep sleep come uppon the Adam, and he took a cell from his body, and he physically closed or "stitched up" the shameful wound down there. The text actually says that. That the first humans were created like malefemales. What today would be called shemales or transsexual. I have reasons to believe that while our Adam stayed human many of the other Adams ascended into angelity, and some of these later stepped down to rape Adams daughters resulting in bizarre creatures, monsters and giants. I also believe that some of the ...
This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to sn
3989 ADAM9, a member of the A Disintegrin And Metalloprotease family of proteins, is a membrane-anchored protein containing an SH3 domain-containing cytoplasmic tail and an extracellular domain comprised of a pro-domain, metalloprotease domain, disintegrin domain, cystein-rich domain, and an epidermal growth factor repeat. ADAM9 has been shown to regulate E-Cadherin internalization and participate in integrin-mediated adhesion processes, and is thought to play a role in tumor aggressiveness. We have developed an ADAM9-specific monoclonal antibody, termed KID24, which is the first reported antibody that inhibits the catalytic activity of ADAM9 in vitro. Immunohistochemical analysis demonstrated KID24 exhibits preferential staining of human tumor tissue over normal tissue. Elevated KID24 staining was observed in lung, colon, pancreatic and prostate adenocarcinomas, confirming previous reports defining ADAM9 as a tumor-associated antigen. ADAM9 is also expressed by a number of Raven cancer stem ...
Weight: The ADAM program uses censuses and propensity scoring to develop sample weights. Sample weights for each location for each year were renormalized so that the sum of all weights equaled the number of cases. This assured that the multi-year analysis would give the appropriate weight to data collected in any given year proportional to the number of cases collected. These weights were used in all statistical calculations to provide unbiased estimates for the target population of adult male arrestees at each location. Data Source: ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2000 (ICPSR 3270). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2001 (ICPSR 3688). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2002 (ICPSR 3815). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2003 (ICPSR 4020). ARRESTEE DRUG ABUSE MONITORING PROGRAM II IN THE UNITED STATES, 2007 (ICPSR 25821). ARRESTEE DRUG ABUSE MONITORING PROGRAM ...
Weight: The ADAM program uses censuses and propensity scoring to develop sample weights. Sample weights for each location for each year were renormalized so that the sum of all weights equaled the number of cases. This assured that the multi-year analysis would give the appropriate weight to data collected in any given year proportional to the number of cases collected. These weights were used in all statistical calculations to provide unbiased estimates for the target population of adult male arrestees at each location. Data Source: ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2000 (ICPSR 3270). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2001 (ICPSR 3688). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2002 (ICPSR 3815). ARRESTEE DRUG ABUSE MONITORING (ADAM) PROGRAM IN THE UNITED STATES, 2003 (ICPSR 4020). ARRESTEE DRUG ABUSE MONITORING PROGRAM II IN THE UNITED STATES, 2007 (ICPSR 25821). ARRESTEE DRUG ABUSE MONITORING PROGRAM ...
Buy anti-ADAMTS2 antibody, Mouse anti-Bovine A Disintegrin And Metalloproteinase With Thrombospondin 2 (ADAMTS2) Monoclonal Antibody-NP_055059.2 (MBS2082091) product datasheet at MyBioSource, Primary Antibodies. Application: Western Blot (WB), Immunocytochemistry (ICC), Immunohistochemistry (IHC), Immunoprecipitation (IP), ELISA (EIA)
This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. Members of the family share several distinct pro
... , Authors: Natacha Rocks, Didier Cataldo. Published in: Atlas Genet Cytogenet Oncol Haematol.
... , Authors: Sawako Yoshina, Shohei Mitani. Published in: Atlas Genet Cytogenet Oncol Haematol.
Prox J, Bernreuther C, Altmeppen H, Grendel J, Glatzel M, DHooge R, Stroobants S, Ahmed T, Balschun D, Willem M, Lammich S, Isbrandt D, Schweizer M, Horré K, De Strooper B, Saftig P. Postnatal Disruption of the Disintegrin/Metalloproteinase ADAM10 in Brain Causes Epileptic Seizures, Learning Deficits, Altered Spine Morphology, and Defective Synaptic Functions ...
Two decades ago, Adam Sharps piano playing led him into a passionate relationship with Angelina Brown, an intelligent and strong-willed actress. They had a chance at something more--but Adam didnt take it.. Now, on the cusp of turning fifty, Adam likes his life. Hes happy with his partner Claire, he excels in music trivia at quiz night at the local pub, he looks after his mother, and he does the occasional consulting job in IT. But he can never quite shake off his nostalgia for what might have been.. And then, out of nowhere, from the other side of the world, Angelina gets in touch. What does she want? Does Adam dare to live dangerously?. Set to the soundtrack of our lives, The Best of Adam Sharp follows along with emotion and humor as one man looks back on his past and decides if having a second chance is worth the risk.. ...
Cannabinoids were shown to induce apoptosis in cells of the neuronal system including neurons, astrocytes, human grade IV astrocytoma, glioma C6, astrocytoma U373-MG, neuroblastoma N18 TG2, and pheochromocytoma PC12 cells and to inhibit proliferation of MCF-7, EFM-19, T47D, and DU145 cells (5 , 26) . On the basis of these findings and their analgesic properties, cannabinoids were suggested as useful drugs to support cancer therapy. Here we show that various cannabinoids potently induce mitogenic kinase signaling in different cancer cell lines. Moreover, we demonstrate, in contrast to other studies that used cannabinoids such as THC at micromolar concentrations, that nanomolar concentrations of THC induce proliferation of cancer cells (Fig. 3, A and B) ⇓ . Importantly, the concentration of THC that was used here is more likely to reflect the therapeutically relevant situation detected in serum after drug treatment (27, 28, 29, 30, 31) .. The binding of cannabinoids to their cognate receptors ...
: ADAMTS-1, -4, -5 and -9 belong to a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family and more precisely to the proteoglycanases subgroup based on their common ability to degrade chondroitin sulfate proteoglycans. They have been extensively investigated for their involvement in inflammation-induced osteoarthritis, and a growing body of evidence indicates that they may be of key importance in the physiological and pathological central nervous system (CNS). In this review, we discuss the deregulated expression of ADAMTS proteoglycanases during acute CNS injuries, such as stroke and spinal cord injury. Then, we provide new insights on ADAMTS proteoglycanases mediating synaptic plasticity, neurorepair, angiogenesis and inflammation mechanisms. Altogether, this review allows us to propose that ADAMTS proteoglycanases may be original therapeutic targets for CNS injuries.
Cleaves the membrane-bound precursor of TNF-alpha to its mature soluble form. Responsible for the proteolytical release of soluble JAM3 from endothelial cells surface (By similarity). Responsible for the proteolytic release of several other cell-surface proteins, including heparin-binding epidermal growth-like factor, ephrin-A2, CD44, CDH2 and for constitutive and regulated alpha-secretase cleavage of amyloid precursor protein (APP) (PubMed:10097139). Contributes to the normal cleavage of the cellular prion protein (By similarity). Involved in the cleavage of the adhesion molecule L1 at the cell surface and in released membrane vesicles, suggesting a vesicle-based protease activity (By similarity). Controls also the proteolytic processing of Notch and mediates lateral inhibition during neurogenesis (By similarity). Responsible for the FasL ectodomain shedding and for the generation of the remnant ADAM10-processed FasL (FasL APL) transmembrane form (By similarity). Also cleaves the ectodomain of the
Complete information for ADAM9 gene (Protein Coding), ADAM Metallopeptidase Domain 9, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Adam slept through the night for the FIRST Time in 16 months on Saturday night! I did not know whether to laugh or cry. It freaked Craig and I out totally! I have told everyone I know that Adam slept through the night. They look at me like I am crazy. I do not think that anyone really understands that he have NEVER slept through the night! I think people, friends, family think we make it up. Everyday at work I have someone talk about how tired they are. I do not think they truly understand what it is like to never get a full nights sleep. We have been very lucky that my in-laws have kept Adam once or twice every week for almost a year. One for us to get sleep and for Jake and matt to get sleep. My mother in law keeps Adam two days a week while I work. As much as we miss him, it does help in keeping some normalcy to our life ...
Adams Inn is an affordable 27-room bed & breakfast centrally located on a quiet, residential street in the Adams Morgan neighborhood. Just one block away lies the commercial and cultural heart of this eclectic neighborhood, with more than 100 of DCs most popular and diverse shops and restaurants. With rates ranging from $79 to $169/night, Adams Inn attracts visitors from all across the country and globe; guests from more than 50 nations have made Adams Inn their home away from home.
Zolkiewska is focusing on ADAM12, which a member of the ADAM family of cell-surface disintegrin-metalloproteases. Unlike other current cancer markers -- which are found in both healthy and cancerous tissues -- ADAM 12 is not expressed in healthy human mammary glands. Zolkiewskas work suggests that ADAM12 is induced precisely in breast cancer stem cells ...
Adam22 - Adam22 (untagged) - Mouse a disintegrin and metallopeptidase domain 22 (Adam22), transcript variant 1, (10ug) available for purchase from OriGene - Your Gene Company.
Myc-DDK-tagged ORF clone of Homo sapiens ADAM metallopeptidase domain 29 (ADAM29), transcript variant 3 as transfection-ready DNA - 10 µg - OriGene - cdna clones
Rabbit polyclonal antibody raised against synthetic peptide of ADAM17. A synthetic peptide corresponding to amino acids 807-823 of human ADAM17. (PAB9716) - Products - Abnova
Fertilin Beta antibody LS-C3520 is an unconjugated mouse monoclonal antibody to mouse Fertilin Beta (ADAM2). Validated for IF and WB.