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Neprilysin
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<h2 id="amyloid-beta-regulation">Amyloid beta regulation</h2> <p>Neprilysin-deficient <a href="/facts/Knockout_mouse/Aw50cobf">knockout mice</a> show both Alzheimer's-like behavioral impairment and amyloid-beta deposition in the brain,<a class="footnote-ref" id="fnref:6" href="#fn:6"><sup>6</sup></a> providing strong evidence for the protein's association with the Alzheimer's disease process. Because neprilysin is thought to be the <a href="/facts/Rate-limiting_step/UC0TNxtX">rate-limiting step</a> in amyloid beta degradation,<a class="footnote-ref" id="fnref:7" href="#fn:7"><sup>7</sup></a> it has been considered a potential therapeutic target; compounds such as the <a href="/facts/Peptide_hormone/8AdC52vt">peptide hormone</a> <a href="/facts/Somatostatin/GAD2utoz">somatostatin</a> have been identified that increase the enzyme's activity level.<a class="footnote-ref" id="fnref:8" href="#fn:8"><sup>8</sup></a> Declining neprilysin activity with increasing age may also be explained by <a href="/facts/Oxidative/Pyd5RVcj">oxidative</a> damage, known to be a causative factor in Alzheimer's disease; higher levels of inappropriately oxidized neprilysin have been found in Alzheimer's patients compared to cognitively normal elderly people.<a class="footnote-ref" id="fnref:9" href="#fn:9"><sup>9</sup></a> </p> <h2 id="signaling-peptides">Signaling peptides</h2> <p>Neprilysin is also associated with other biochemical processes, and is particularly highly expressed in <a href="/facts/Kidney/HBspPrv9">kidney</a> and <a href="/facts/Lung/gTWXI6Fj">lung</a> tissues. Inhibitors have been designed with the aim of developing <a href="/facts/Analgesic/xLj4XBcq">analgesic</a> and <a href="/facts/Antihypertensive/K63MbxN0">antihypertensive</a> agents that act by preventing neprilysin's activity against signaling peptides such as <a href="/facts/Enkephalin/lVvearbQ">enkephalins</a>, <a href="/facts/Substance_P/BySc2oeD">substance P</a>, <a href="/facts/Endothelin/V4pSN8x0">endothelin</a>, and <a href="/facts/Atrial_natriuretic_peptide/Vc4NAsIF">atrial natriuretic peptide</a>.<a class="footnote-ref" id="fnref:10" href="#fn:10"><sup>10</sup></a><a class="footnote-ref" id="fnref:11" href="#fn:11"><sup>11</sup></a> </p><p>Associations have been observed between neprilysin expression and various types of <a href="/facts/Cancer/PVW6n1D0">cancer</a>; however, the relationship between neprilysin expression and carcinogenesis remains obscure. In cancer <a href="/facts/Biomarker/nk2LgXtq">biomarker</a> studies, the neprilysin gene is often referred to as CD10 or CALLA. In some types of cancer, such as <a href="/facts/Metastatic/4dadbm6z">metastatic</a> <a href="/facts/Carcinoma/NE9UY4VB">carcinoma</a> and some advanced <a href="/facts/Melanoma/qdT7E97Y">melanomas</a>, neprilysin is overexpressed;<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a> in other types, most notably <a href="/facts/Lung_cancer/LHLdR454">lung cancers</a>, neprilysin is downregulated, and thus unable to modulate the pro-growth <a href="/facts/Autocrine/EwfQEYzG">autocrine</a> signaling of cancer cells via secreted peptides such as mammalian <a href="/facts/Homology_(biology)/muctKlyT">homologs</a> related to <a href="/facts/Bombesin/1vYqaFWH">bombesin</a>.<a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a> Some plant extracts (methanol extracts of <i><a href="/facts/Ceropegia/FoDgo6Sx">Ceropegia</a> rupicola</i>, <i><a href="/facts/Kniphofia/hqAs711t">Kniphofia</a> sumarae</i>, <i> <a href="/facts/Plectranthus/sUKyJaSC">Plectranthus</a> cf barbatus</i>, and an aqueous extract of <i><a href="/facts/Pavetta/SC1Yqg2t">Pavetta</a> longiflora</i>) were found able to inhibit the enzymatic activity of neutral endopeptidase.<a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> </p> <h2 id="inhibitors">Inhibitors</h2> <p>Inhibitors have been designed with the aim of developing <a href="/facts/Analgesic/xLj4XBcq">analgesic</a> and <a href="/facts/Antihypertensive/K63MbxN0">antihypertensive</a> agents that act by preventing neprilysin's activity against signaling peptides such as <a href="/facts/Enkephalin/lVvearbQ">enkephalins</a>, <a href="/facts/Substance_P/BySc2oeD">substance P</a>, <a href="/facts/Endothelin/V4pSN8x0">endothelin</a>, and <a href="/facts/Atrial_natriuretic_peptide/Vc4NAsIF">atrial natriuretic peptide</a>.<a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a><a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a> </p><p>Some are intended to treat <a href="/facts/Heart_failure/7fckX3Jm">heart failure</a>.<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a> </p> <ul><li><a href="/facts/Sacubitril/valsartan/mJ1krlNA">Sacubitril/valsartan</a> (Entresto/LCZ696), which has been tested against <a href="/facts/Enalapril/b4Wr1lWN">enalapril</a> in patients with heart failure.<a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a></li> <li><a href="/facts/Sacubitril/0u9hUlgK">Sacubitril</a> (AHU-377), a <a href="/facts/Prodrug/cg0GNhH0">prodrug</a> which is a component of <a href="/facts/Sacubitril/valsartan/mJ1krlNA">sacubitril/valsartan</a></li> <li><a href="/facts/Sacubitrilat/lBGdE5sx">Sacubitrilat</a> (LBQ657), the active form of sacubitril</li> <li><a href="/facts/RB-101/RwdDssaF">RB-101</a>, an enkephalinase inhibitor, used in scientific research.</li> <li><a href="/facts/UK-414,495/eMI1WQy1">UK-414,495</a></li> <li><a href="/facts/Omapatrilat/tpkB5QP7">Omapatrilat</a> (dual inhibitor of NEP and <a href="/facts/Angiotensin-converting_enzyme/n6hlpyJh">angiotensin-converting enzyme</a>) developed by BMS did not receive FDA approval due to <a href="/facts/Angioedema/Wpc7qnTK">angioedema</a> safety concerns.</li> <li><a href="/facts/Ecadotril/JQX3kybY">Ecadotril</a></li> <li><a href="/facts/Candoxatril/nz1QMkxb">Candoxatril</a></li></ul> <p>Other dual inhibitors of NEP with ACE/angiotensin receptor were (in 2003) being developed by pharmaceutical companies.<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a> </p> <h2 id="immunochemistry">Immunochemistry</h2> <p>CD10 is used in clinical pathology for diagnostic purpose. </p> <h3>In lymphomas and leukemias</h3> <ul><li><a href="/facts/Acute_lymphoblastic_leukemia/vRIAjkRJ">Acute lymphoblastic leukemia</a> (ALL) cells are CD10+.</li> <li><a href="/facts/Follicular_lymphoma/Ntaq19Ea">Follicular lymphoma</a> (follicle centre cell lymphoma) are CD10+.</li> <li>Burkitt Lymphoma cells are CD10+.</li> <li>CD10+ diffuse large B cell lymphoma (CD10+ DLBCL)<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> <ul><li>Marker for germinal center phenotype (CD10, HGAL, BCL6, CD38) are considered a favorable prognostic factor,<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a><a class="footnote-ref" id="fnref:22" href="#fn:22"><sup>22</sup></a> but CD10+, <a href="/facts/BCL2/I34R1guW">BCL2</a>+ tumors could have poorer survival.<a class="footnote-ref" id="fnref:23" href="#fn:23"><sup>23</sup></a> For some authors, CD10 expression in DLBCL does not influence survival.<a class="footnote-ref" id="fnref:24" href="#fn:24"><sup>24</sup></a></li></ul></li> <li><a href="/facts/Angioimmunoblastic_T_cell_lymphoma/5XleScmv">Angioimmunoblastic T cell lymphoma</a> (AITL) are CD10+<a class="footnote-ref" id="fnref:25" href="#fn:25"><sup>25</sup></a><a class="footnote-ref" id="fnref:26" href="#fn:26"><sup>26</sup></a> and distinguishes AITL from other T cell lymphomas (CD10−)<a class="footnote-ref" id="fnref:27" href="#fn:27"><sup>27</sup></a> <ul><li>Some benign T cells can be CD10+<a class="footnote-ref" id="fnref:28" href="#fn:28"><sup>28</sup></a></li></ul></li></ul> <h3>In epithelial tumors</h3> <ul><li><a href="/facts/Clear_cell_renal_cell_carcinoma/p5kjjtrw">Clear cell renal cell carcinoma</a> (Clear cell RCC) <ul><li>CD10+ distinguishes renal cell carcinoma, conventional type with eosinophilic morphology from its mimickers. Chromophobe carcinoma and oncocytoma are CD10−.<a class="footnote-ref" id="fnref:29" href="#fn:29"><sup>29</sup></a></li></ul></li> <li><a href="/facts/Pancreatic_tumor/SPclnt3q">Pancreatic tumors</a> <ul><li><a href="/facts/Solid_pseudopapillary_tumour/25r2mxET">Solid pseudopapillary tumours</a> are CD10+.<a class="footnote-ref" id="fnref:30" href="#fn:30"><sup>30</sup></a></li> <li>CD10+ differentiates <a href="/facts/Mucinous_cystic_neoplasm/MTMGD28e">mucinous cystic neoplasms</a> (CD10+/CK20+) from <a href="/facts/Intraductal_papillary_mucinous_neoplasm/cWW2sw7j">intraductal papillary mucinous neoplasm</a> of branch duct type (CD10−/CK20-).<a class="footnote-ref" id="fnref:31" href="#fn:31"><sup>31</sup></a></li></ul></li> <li>Cutaneous tumors <ul><li>CD10 may differentiate <a href="/facts/Basal_cell_carcinoma/NLHsYND7">basal cell carcinoma</a> (CD10 epithelial staining) from <a href="/facts/Trichoblastoma/g6nI68Fy">trichoblastoma</a> (CD10 peritumoral stromal staining), basal cell carcinoma with follicular differentiation (CD10 stromal and epithelial staining)<a class="footnote-ref" id="fnref:32" href="#fn:32"><sup>32</sup></a> and <a href="/facts/Squamous_cell_carcinoma/AkoAvh1P">squamous cell carcinoma</a> (strong stromal staining).<a class="footnote-ref" id="fnref:33" href="#fn:33"><sup>33</sup></a></li> <li>CD10 differentiates CD10+ <a href="/facts/Atypical_fibroxanthoma/Po0BjBd2">atypical fibroxanthoma</a> from CD10− spindle cell <a href="/facts/Melanoma/qdT7E97Y">melanoma</a> and sarcomatoid <a href="/facts/Squamous_cell_carcinoma/AkoAvh1P">squamous cell carcinoma</a>.</li></ul></li> <li>Urothelial tumors express CD10 (42-67%).<a class="footnote-ref" id="fnref:34" href="#fn:34"><sup>34</sup></a> <ul><li>CD10 expression is strongly correlated with high tumor grade and stage in urothelial carcinoma of the bladder. CD10 may be associated with tumor progression in bladder cancer pathogenesis.<a class="footnote-ref" id="fnref:35" href="#fn:35"><sup>35</sup></a></li></ul></li></ul> <h3>In other tumors</h3> <ul><li>CD10 expression might be one of the characteristics of müllerian system-derived neoplastic mesenchymal cells.<a class="footnote-ref" id="fnref:36" href="#fn:36"><sup>36</sup></a> <ul><li>Normal endometrial stroma<a class="footnote-ref" id="fnref:37" href="#fn:37"><sup>37</sup></a></li> <li><a href="/facts/Endometrial_stromal_sarcoma/nyswoAJj">Endometrial stromal sarcoma</a> (ESS) are CD10+ (<a href="/facts/Smooth_muscle_tumor/5VP2KR4h">Smooth muscle tumors</a> are usually CD10−,<a class="footnote-ref" id="fnref:38" href="#fn:38"><sup>38</sup></a> but can be CD10+<a class="footnote-ref" id="fnref:39" href="#fn:39"><sup>39</sup></a></li> <li>Malignant müllerian mixed tumor (MMMT)</li> <li>Müllerian adenosarcoma</li> <li>Uterine high-grade leiomyosarcoma</li> <li>Uterine rhabdomyosarcoma</li></ul></li> <li>Vascular tumors <ul><li><a href="/facts/Epithelioid_hemangioendothelioma/VhSyf7xA">Epithelioid hemangioendothelioma</a> are mostly CD10+.<a class="footnote-ref" id="fnref:40" href="#fn:40"><sup>40</sup></a></li> <li><a href="/facts/Hemangioblastoma/WV56Cjq2">Hemangioblastoma</a> is usually CD10− (metastatic <a href="/facts/Renal_cell_carcinoma/rRXSrA63">renal cell carcinoma</a> is CD10+)<a class="footnote-ref" id="fnref:41" href="#fn:41"><sup>41</sup></a><a class="footnote-ref" id="fnref:42" href="#fn:42"><sup>42</sup></a></li></ul></li></ul> <h2 id="see-also">See also</h2> <ul><li><a href="/facts/List_of_histologic_stains_that_aid_in_diagnosis_of_cutaneous_conditions/BggvlboG">List of histologic stains that aid in diagnosis of cutaneous conditions</a></li></ul> <h2 id="external-links">External links</h2> <ul><li>The <a href="/facts/MEROPS/kgboIz3H">MEROPS</a> online database for peptidases and their inhibitors: <a href="http://merops.sanger.ac.uk/cgi-bin/merops.cgi?id=M13.001">M13.001</a></li> <li><a href="https://meshb.nlm.nih.gov/record/ui?name=Neprilysin">Neprilysin</a> at the U.S. National Library of Medicine <a href="/facts/Medical_Subject_Headings/C57g2JuF">Medical Subject Headings</a> (MeSH)</li> <li>Overview of all the structural information available in the <a href="/facts/Protein_Data_Bank/oUhq4ABD">PDB</a> for <a href="/facts/UniProt/lfDDHjAl">UniProt</a>: <i><a href="https://www.ebi.ac.uk/pdbe/pdbe-kb/proteins/P08473">P08473</a></i> (Neprilysin) at the <a href="/facts/PDBe-KB/p1WX7lPH">PDBe-KB</a>.</li></ul> <p><i>This article incorporates text from the <a href="/facts/United_States_National_Library_of_Medicine/Hzty0MCX">United States National Library of Medicine</a>, which is in the <a href="/facts/Public_domain/YWKMDKw4">public domain</a>.</i> </p> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>"Entrez Gene: Membrane metallo-endopeptidase". <a href="https://www.ncbi.nlm.nih.gov/gene/4311" target="_blank">https://www.ncbi.nlm.nih.gov/gene/4311</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>"Entrez Gene: Membrane metallo-endopeptidase". <a href="https://www.ncbi.nlm.nih.gov/gene/4311" target="_blank">https://www.ncbi.nlm.nih.gov/gene/4311</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Galy A, Travis M, Cen D, Chen B (October 1995). "Human T, B, natural killer, and dendritic cells arise from a common bone marrow progenitor cell subset". Immunity. 3 (4): 459–473. doi:10.1016/1074-7613(95)90175-2. PMID 7584137. <a href="https://doi.org/10.1016%2F1074-7613%2895%2990175-2" target="_blank">https://doi.org/10.1016%2F1074-7613%2895%2990175-2</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Singh C (2011-02-25). "CD10". CD Markers. PathologyOutlines.com, Inc. <a href="http://www.pathologyoutlines.com/topic/cdmarkerscd10.html" target="_blank">http://www.pathologyoutlines.com/topic/cdmarkerscd10.html</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>Papandreou CN, Nanus DM (January 2010). "Is methylation the key to CD10 loss?". J. Pediatr. Hematol. Oncol. 32 (1): 2–3. doi:10.1097/MPH.0b013e3181c74aca. PMID 20051779. <a href="https://doi.org/10.1097%2FMPH.0b013e3181c74aca" target="_blank">https://doi.org/10.1097%2FMPH.0b013e3181c74aca</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Madani R, Poirier R, Wolfer DP, Welzl H, Groscurth P, Lipp HP, et al. (December 2006). "Lack of neprilysin suffices to generate murine amyloid-like deposits in the brain and behavioral deficit in vivo". J. Neurosci. Res. 84 (8): 1871–8. doi:10.1002/jnr.21074. PMID 16998901. S2CID 46527377. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Iwata N, Tsubuki S, Takaki Y, Watanabe K, Sekiguchi M, Hosoki E, et al. (February 2000). "Identification of the major Abeta1-42-degrading catabolic pathway in brain parenchyma: suppression leads to biochemical and pathological deposition". Nat. Med. 6 (2): 143–50. doi:10.1038/72237. PMID 10655101. S2CID 22431826. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> <li id="fn:8"><p>Iwata N, Higuchi M, Saido TC (November 2005). "Metabolism of amyloid-beta peptide and Alzheimer's disease". Pharmacol. Ther. 108 (2): 129–48. doi:10.1016/j.pharmthera.2005.03.010. PMID 16112736. <a href="https://doi.org/10.1016%2Fj.pharmthera.2005.03.010" target="_blank">https://doi.org/10.1016%2Fj.pharmthera.2005.03.010</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></p></li> <li id="fn:9"><p>Wang DS, Iwata N, Hama E, Saido TC, Dickson DW (October 2003). "Oxidized neprilysin in aging and Alzheimer's disease brains". Biochem. Biophys. Res. Commun. 310 (1): 236–41. doi:10.1016/j.bbrc.2003.09.003. PMID 14511676. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></p></li> <li id="fn:10"><p>Sahli S, Stump B, Welti T, Schweizer WB, Diederich R, Blum-Kaelin D, et al. (April 2005). "A New Class of Inhibitors for the Metalloprotease Neprilysin Based on a Central Imidazole Scaffold". Helvetica Chimica Acta. 88 (4): 707–730. doi:10.1002/hlca.200590050. <a href="https://doi.org/10.1002%2Fhlca.200590050" target="_blank">https://doi.org/10.1002%2Fhlca.200590050</a> <a href="#fnref:10" class="footnote-back-ref">↩</a></p></li> <li id="fn:11"><p>Oefner C, Roques BP, Fournie-Zaluski MC, Dale GE (February 2004). "Structural analysis of neprilysin with various specific and potent inhibitors". Acta Crystallogr. D. 60 (Pt 2): 392–6. doi:10.1107/S0907444903027410. PMID 14747736. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:11" class="footnote-back-ref">↩</a></p></li> <li id="fn:12"><p>Velazquez EF, Yancovitz M, Pavlick A, Berman R, Shapiro R, Bogunovic D, et al. (2007). "Clinical relevance of neutral endopeptidase (NEP/CD10) in melanoma". J Transl Med. 5 (1): 2. doi:10.1186/1479-5876-5-2. PMC 1770905. PMID 17207277. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770905" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770905</a> <a href="#fnref:12" class="footnote-back-ref">↩</a></p></li> <li id="fn:13"><p>Cohen AJ, Bunn PA, Franklin W, Magill-Solc C, Hartmann C, Helfrich B, et al. (February 1996). "Neutral endopeptidase: variable expression in human lung, inactivation in lung cancer, and modulation of peptide-induced calcium flux". Cancer Res. 56 (4): 831–9. PMID 8631021. <a href="http://cancerres.aacrjournals.org/cgi/reprint/56/4/831" target="_blank">http://cancerres.aacrjournals.org/cgi/reprint/56/4/831</a> <a href="#fnref:13" class="footnote-back-ref">↩</a></p></li> <li id="fn:14"><p>Alasbahi R, Melzig MF (January 2008). "Screening of some Yemeni medicinal plants for inhibitory activity against peptidases". Pharmazie. 63 (1): 86–8. doi:10.1055/s-2008-1047849. PMID 18271311. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:14" class="footnote-back-ref">↩</a></p></li> <li id="fn:15"><p>Sahli S, Stump B, Welti T, Schweizer WB, Diederich R, Blum-Kaelin D, et al. (April 2005). "A New Class of Inhibitors for the Metalloprotease Neprilysin Based on a Central Imidazole Scaffold". Helvetica Chimica Acta. 88 (4): 707–730. doi:10.1002/hlca.200590050. <a href="https://doi.org/10.1002%2Fhlca.200590050" target="_blank">https://doi.org/10.1002%2Fhlca.200590050</a> <a href="#fnref:15" class="footnote-back-ref">↩</a></p></li> <li id="fn:16"><p>Oefner C, Roques BP, Fournie-Zaluski MC, Dale GE (February 2004). "Structural analysis of neprilysin with various specific and potent inhibitors". Acta Crystallogr. D. 60 (Pt 2): 392–6. doi:10.1107/S0907444903027410. PMID 14747736. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:16" class="footnote-back-ref">↩</a></p></li> <li id="fn:17"><p>McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, et al. (Sep 2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". The New England Journal of Medicine. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. hdl:10993/27659. PMID 25176015. 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