The H + Transporter SLC4A11: Roles in Metabolism, Oxidative Stress and Mitochondrial Uncoupling
Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H transporter activated by NH and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of the SLC4 family. SLC4A11 mutations can lead to corn...
Saved in:
| Published in: | Cells (Basel, Switzerland) Vol. 11; no. 2; p. 197 |
|---|---|
| Main Authors: | , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Switzerland
MDPI AG
07-01-2022
MDPI |
| Subjects: | |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Abstract | Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H
transporter activated by NH
and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of the SLC4 family. SLC4A11 mutations can lead to corneal endothelial dystrophy and hearing deficits that are recapitulated in SLC4A11 knock-out mice. SLC4A11, at the inner mitochondrial membrane, facilitates glutamine catabolism and suppresses the production of mitochondrial superoxide by providing ammonia-sensitive H
uncoupling that reduces glutamine-driven mitochondrial membrane potential hyperpolarization. Mitochondrial oxidative stress in SLC4A11 KO also triggers dysfunctional autophagy and lysosomes, as well as ER stress. SLC4A11 expression is induced by oxidative stress through the transcription factor NRF2, the master regulator of antioxidant genes. Outside of the corneal endothelium, SLC4A11's function has been demonstrated in cochlear fibrocytes, salivary glands, and kidneys, but is largely unexplored overall. Increased SLC4A11 expression is a component of some "glutamine-addicted" cancers, and is possibly linked to cells and tissues that rely on glutamine catabolism. |
|---|---|
| AbstractList | Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H+ transporter activated by NH3 and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of the SLC4 family. SLC4A11 mutations can lead to corneal endothelial dystrophy and hearing deficits that are recapitulated in SLC4A11 knock-out mice. SLC4A11, at the inner mitochondrial membrane, facilitates glutamine catabolism and suppresses the production of mitochondrial superoxide by providing ammonia-sensitive H+ uncoupling that reduces glutamine-driven mitochondrial membrane potential hyperpolarization. Mitochondrial oxidative stress in SLC4A11 KO also triggers dysfunctional autophagy and lysosomes, as well as ER stress. SLC4A11 expression is induced by oxidative stress through the transcription factor NRF2, the master regulator of antioxidant genes. Outside of the corneal endothelium, SLC4A11’s function has been demonstrated in cochlear fibrocytes, salivary glands, and kidneys, but is largely unexplored overall. Increased SLC4A11 expression is a component of some “glutamine-addicted” cancers, and is possibly linked to cells and tissues that rely on glutamine catabolism. Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H + transporter activated by NH 3 and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of the SLC4 family. SLC4A11 mutations can lead to corneal endothelial dystrophy and hearing deficits that are recapitulated in SLC4A11 knock-out mice. SLC4A11, at the inner mitochondrial membrane, facilitates glutamine catabolism and suppresses the production of mitochondrial superoxide by providing ammonia-sensitive H + uncoupling that reduces glutamine-driven mitochondrial membrane potential hyperpolarization. Mitochondrial oxidative stress in SLC4A11 KO also triggers dysfunctional autophagy and lysosomes, as well as ER stress. SLC4A11 expression is induced by oxidative stress through the transcription factor NRF2, the master regulator of antioxidant genes. Outside of the corneal endothelium, SLC4A11’s function has been demonstrated in cochlear fibrocytes, salivary glands, and kidneys, but is largely unexplored overall. Increased SLC4A11 expression is a component of some “glutamine-addicted” cancers, and is possibly linked to cells and tissues that rely on glutamine catabolism. Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H transporter activated by NH and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of the SLC4 family. SLC4A11 mutations can lead to corneal endothelial dystrophy and hearing deficits that are recapitulated in SLC4A11 knock-out mice. SLC4A11, at the inner mitochondrial membrane, facilitates glutamine catabolism and suppresses the production of mitochondrial superoxide by providing ammonia-sensitive H uncoupling that reduces glutamine-driven mitochondrial membrane potential hyperpolarization. Mitochondrial oxidative stress in SLC4A11 KO also triggers dysfunctional autophagy and lysosomes, as well as ER stress. SLC4A11 expression is induced by oxidative stress through the transcription factor NRF2, the master regulator of antioxidant genes. Outside of the corneal endothelium, SLC4A11's function has been demonstrated in cochlear fibrocytes, salivary glands, and kidneys, but is largely unexplored overall. Increased SLC4A11 expression is a component of some "glutamine-addicted" cancers, and is possibly linked to cells and tissues that rely on glutamine catabolism. |
| Author | Bonanno, Joseph A Ogando, Diego G Shyam, Raji Choi, Moonjung |
| AuthorAffiliation | Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA; rashyam@iu.edu (R.S.); choimoon@iu.edu (M.C.).; digogand@iu.edu (D.G.O.) |
| AuthorAffiliation_xml | – name: Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA; rashyam@iu.edu (R.S.); choimoon@iu.edu (M.C.).; digogand@iu.edu (D.G.O.) |
| Author_xml | – sequence: 1 givenname: Joseph A orcidid: 0000-0002-3842-7646 surname: Bonanno fullname: Bonanno, Joseph A organization: Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA – sequence: 2 givenname: Raji orcidid: 0000-0003-2154-4173 surname: Shyam fullname: Shyam, Raji organization: Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA – sequence: 3 givenname: Moonjung orcidid: 0000-0002-7218-4924 surname: Choi fullname: Choi, Moonjung organization: Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA – sequence: 4 givenname: Diego G surname: Ogando fullname: Ogando, Diego G organization: Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35053313$$D View this record in MEDLINE/PubMed |
| BookMark | eNpdks9rFDEUgINUbK09epWAF6GO5udk4kEoi9rCloJdzyGTvNnNMptsk5li_3tn3Vq65pKQfPnyXt57jY5iioDQW0o-ca7JZwd9XygljFCtXqATRhSvhCD66Nn6GJ2VsibTaGhNiXyFjrkkknPKT5BZrABf4nO8yDaWbcoDZHw7n4kLSr_gn6mHgkPE1zDYNvWhbD7im9_B2yHcA74dMpSCbfT4OgzJrVL0Odge_4oujds-xOUb9LKzfYGzx_kULb5_W8wuq_nNj6vZxbxyUqihclQ7C5KprlWM00ZCo4ExLRTttNDWqtZ3nWCdpMQK3UwYl8J73gpWa8JP0dVe65Ndm20OG5sfTLLB_N1IeWlsHoLrwXBqpfPCT_ca0XCwwBthoWWtlrSxfHJ93bu2Y7sB7yAO2fYH0sOTGFZmme5NoxQXtZwEHx4FOd2NUAazCWVXKhshjcWwmjE2vV2rCX3_H7pOY47TT-0oypRQaies9pTLqZQM3VMwlJhdI5iDRpj4d88zeKL_lZ3_ARFurvs |
| CitedBy_id | crossref_primary_10_1007_s00432_023_04592_7 crossref_primary_10_3389_fphar_2022_905501 crossref_primary_10_14814_phy2_15535 crossref_primary_10_3390_cancers15164058 crossref_primary_10_3390_ijms23116333 crossref_primary_10_1016_j_xops_2022_100212 crossref_primary_10_1021_acs_jmedchem_3c00238 crossref_primary_10_3390_cells12111528 crossref_primary_10_3390_ijms242015166 crossref_primary_10_1167_iovs_65_4_18 |
| Cites_doi | 10.1016/j.xops.2021.100084 10.1097/ICO.0000000000001775 10.1167/iovs.17-21781 10.1038/s41598-019-46094-y 10.14814/phy2.14089 10.1021/bi101887z 10.1016/j.molcel.2004.09.030 10.1167/iovs.62.7.28 10.1152/ajpcell.00271.2014 10.1167/iovs.13-11929 10.1038/bjc.2017.113 10.1038/ajg.2011.123 10.1167/iovs.08-3006 10.1152/ajpcell.00259.2016 10.1016/j.mam.2012.10.008 10.1167/iovs.15-17802 10.1152/ajpcell.00425.2019 10.1152/ajpcell.00056.2013 10.1074/jbc.RA119.009093 10.1167/iovs.61.2.7 10.1093/hmg/ddm337 10.1152/ajpregu.00356.2007 10.1093/hmg/ddt307 10.1152/ajpcell.00309.2016 10.1152/ajpcell.00078.2016 10.1002/humu.21356 10.1002/humu.22601 10.1080/13816810701850033 10.1002/humu.23401 10.1097/ICO.0000000000000421 10.1152/ajpcell.00233.2016 10.1038/nature10642 10.1016/j.exer.2018.12.003 10.1016/j.freeradbiomed.2011.06.022 10.1136/jmg.2006.044644 10.1167/iovs.61.8.39 10.1038/ng1824 10.1016/j.redox.2019.101260 10.1167/iovs.62.12.15 10.1152/ajpcell.00095.2016 10.2353/ajpath.2010.100279 10.1371/journal.pone.0187385 10.1007/s00709-021-01677-3 10.1113/JP272796 10.1006/bbrc.2001.4692 10.1038/s41598-017-03654-4 10.1245/s10434-020-08498-3 10.1016/j.exer.2021.108884 10.1074/jbc.M109.094680 10.1002/humu.21655 10.1001/archopht.126.5.700 10.1074/jbc.M114.627455 10.1152/ajpcell.00246.2015 10.1167/iovs.18-24301 10.1097/ICO.0b013e318074bb01 10.1167/iovs.62.12.4 10.14814/phy2.14232 10.4161/cc.4.1.1394 10.1097/ICO.0000000000000041 10.1172/JCI69600 10.1038/nrc.2016.71 10.1016/j.ebiom.2017.01.004 10.1186/1750-1172-3-28 10.1167/iovs.13-12089 10.1074/jbc.M109.008102 10.1016/j.jmb.2018.03.025 10.1016/j.freeradbiomed.2021.03.006 10.3390/jcm10091979 10.1097/ICO.0000000000002183 |
| ContentType | Journal Article |
| Copyright | 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2022 by the authors. 2022 |
| Copyright_xml | – notice: 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2022 by the authors. 2022 |
| DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 8FD 8FE 8FH ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FR3 GNUQQ HCIFZ LK8 M7P P64 PIMPY PQEST PQQKQ PQUKI PRINS RC3 7X8 5PM DOA |
| DOI | 10.3390/cells11020197 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef Technology Research Database ProQuest SciTech Collection ProQuest Natural Science Collection ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central ProQuest Natural Science Collection ProQuest One Community College ProQuest Central Engineering Research Database ProQuest Central Student SciTech Premium Collection (Proquest) (PQ_SDU_P3) Biological Sciences Biological Science Database Biotechnology and BioEngineering Abstracts Publicly Available Content Database ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) Directory of Open Access Journals |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef Publicly Available Content Database ProQuest Central Student Technology Research Database ProQuest Biological Science Collection ProQuest Central Essentials ProQuest One Academic Eastern Edition ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection Biological Science Database ProQuest SciTech Collection ProQuest Central China Biotechnology and BioEngineering Abstracts ProQuest Central Genetics Abstracts ProQuest One Academic UKI Edition Natural Science Collection ProQuest Central Korea Biological Science Collection Engineering Research Database ProQuest One Academic MEDLINE - Academic |
| DatabaseTitleList | Publicly Available Content Database MEDLINE - Academic MEDLINE CrossRef |
| Database_xml | – sequence: 1 dbid: DOA name: Directory of Open Access Journals url: http://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: ECM name: MEDLINE url: https://search.ebscohost.com/login.aspx?direct=true&db=cmedm&site=ehost-live sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2073-4409 |
| ExternalDocumentID | oai_doaj_org_article_31a5cd4d2698483eae384aeb2b9518a3 10_3390_cells11020197 35053313 |
| Genre | Journal Article Review Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: NEI NIH HHS grantid: R01 EY008834 – fundername: NEI NIH HHS grantid: R01 EY031321 – fundername: NIH HHS grantid: 5R01EY031321 |
| GroupedDBID | 53G 5VS 8FE 8FH AADQD AAFWJ ABDBF ADBBV AFKRA AFPKN AFZYC ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BBNVY BCNDV BENPR BHPHI CCPQU CGR CUY CVF DIK EBD ECM EIF ESX GROUPED_DOAJ HCIFZ HYE IAO IHR ITC KQ8 LK8 M48 M7P MODMG M~E NPM OK1 PGMZT PIMPY PROAC RIG RPM AAYXX CITATION 8FD ABUWG AZQEC DWQXO FR3 GNUQQ P64 PQEST PQQKQ PQUKI PRINS RC3 7X8 5PM |
| ID | FETCH-LOGICAL-c547t-c19cae527fb723185e89e229471f949aa7bdff42f510a498fb7354dd3b426903 |
| IEDL.DBID | RPM |
| ISSN | 2073-4409 |
| IngestDate | Tue Oct 22 15:15:32 EDT 2024 Tue Sep 17 21:27:45 EDT 2024 Sat Aug 17 05:32:58 EDT 2024 Thu Oct 10 16:50:28 EDT 2024 Fri Aug 23 04:37:25 EDT 2024 Sat Nov 02 12:17:37 EDT 2024 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | ammonia MCT4 glutamine lactate corneal endothelial dystrophy |
| Language | English |
| License | Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c547t-c19cae527fb723185e89e229471f949aa7bdff42f510a498fb7354dd3b426903 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-2 |
| ORCID | 0000-0003-2154-4173 0000-0002-3842-7646 0000-0002-7218-4924 |
| OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8773465/ |
| PMID | 35053313 |
| PQID | 2621274775 |
| PQPubID | 2032536 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_31a5cd4d2698483eae384aeb2b9518a3 pubmedcentral_primary_oai_pubmedcentral_nih_gov_8773465 proquest_miscellaneous_2622284867 proquest_journals_2621274775 crossref_primary_10_3390_cells11020197 pubmed_primary_35053313 |
| PublicationCentury | 2000 |
| PublicationDate | 20220107 |
| PublicationDateYYYYMMDD | 2022-01-07 |
| PublicationDate_xml | – month: 1 year: 2022 text: 20220107 day: 7 |
| PublicationDecade | 2020 |
| PublicationPlace | Switzerland |
| PublicationPlace_xml | – name: Switzerland – name: Basel |
| PublicationTitle | Cells (Basel, Switzerland) |
| PublicationTitleAlternate | Cells |
| PublicationYear | 2022 |
| Publisher | MDPI AG MDPI |
| Publisher_xml | – name: MDPI AG – name: MDPI |
| References | Li (ref_43) 2019; 180 Romero (ref_5) 2013; 34 Malhotra (ref_20) 2019; 9 Alka (ref_42) 2018; 59 ref_55 Kao (ref_3) 2016; 311 Yang (ref_38) 2019; 7 Ogando (ref_52) 2021; 62 Chiu (ref_57) 2015; 56 Nehrke (ref_58) 2016; 311 Groger (ref_32) 2010; 285 Vilas (ref_17) 2012; 33 Roy (ref_65) 2015; 34 Vithana (ref_13) 2008; 17 Davuluri (ref_64) 2016; 594 Gee (ref_36) 2019; 7 Hemadevi (ref_25) 2008; 126 Ogando (ref_46) 2019; 26 Desir (ref_30) 2008; 3 Hensley (ref_68) 2013; 123 Vilas (ref_15) 2013; 22 Shyam (ref_47) 2021; 62 Kao (ref_9) 2020; 318 Damkier (ref_4) 2007; 293 Li (ref_49) 2016; 311 Ogando (ref_51) 2021; 214 Jurkunas (ref_28) 2018; 37 Montoliu (ref_61) 2011; 106 Still (ref_69) 2017; 116 Sultana (ref_23) 2007; 13 Jurkunas (ref_29) 2010; 177 Lopez (ref_31) 2009; 284 Berry (ref_62) 2018; 430 Mailloux (ref_63) 2011; 51 Loganathan (ref_14) 2016; 310 Myers (ref_54) 2016; 311 Parker (ref_1) 2001; 282 Jalimarada (ref_10) 2013; 54 Vithana (ref_21) 2006; 38 Guha (ref_27) 2017; 7 Zhang (ref_56) 2017; 58 Park (ref_18) 2005; 4 Choi (ref_37) 2021; 62 Li (ref_50) 2020; 61 Loganathan (ref_11) 2016; 311 Zhang (ref_45) 2017; 16 Loganathan (ref_40) 2014; 35 Ogando (ref_12) 2013; 305 Zhang (ref_53) 2015; 290 Siddiqui (ref_33) 2014; 33 Alka (ref_41) 2018; 39 Guha (ref_66) 2021; 167 Sandoval (ref_59) 2019; 294 Riazuddin (ref_39) 2010; 31 Altman (ref_67) 2016; 16 Aldave (ref_22) 2007; 26 Chaurasia (ref_34) 2020; 39 Aldahmesh (ref_26) 2009; 50 Shinto (ref_70) 2020; 27 Shah (ref_24) 2008; 29 Han (ref_35) 2013; 54 Jiao (ref_8) 2007; 44 ref_48 Vilas (ref_2) 2011; 50 Mullen (ref_60) 2011; 481 ref_7 Zhang (ref_44) 2020; 61 ref_6 Kao (ref_16) 2015; 308 Park (ref_19) 2004; 16 |
| References_xml | – ident: ref_48 doi: 10.1016/j.xops.2021.100084 – volume: 37 start-page: S50 year: 2018 ident: ref_28 article-title: Fuchs Endothelial Corneal Dystrophy Through the Prism of Oxidative Stress publication-title: Cornea doi: 10.1097/ICO.0000000000001775 contributor: fullname: Jurkunas – volume: 58 start-page: 3723 year: 2017 ident: ref_56 article-title: Conditionally Immortal Slc4a11−/− Mouse Corneal Endothelial Cell Line Recapitulates Disrupted Glutaminolysis Seen in Slc4a11−/− Mouse Model publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.17-21781 contributor: fullname: Zhang – volume: 9 start-page: 9681 year: 2019 ident: ref_20 article-title: Human Corneal Expression of SLC4A11, a Gene Mutated in Endothelial Corneal Dystrophies publication-title: Sci. Rep. doi: 10.1038/s41598-019-46094-y contributor: fullname: Malhotra – volume: 7 start-page: e14089 year: 2019 ident: ref_36 article-title: Expression of SLC4A11 protein in mouse and rat medulla: A candidate transporter involved in outer medullary ammonia recycling publication-title: Physiol. Rep. doi: 10.14814/phy2.14089 contributor: fullname: Gee – volume: 50 start-page: 2157 year: 2011 ident: ref_2 article-title: A biochemical framework for SLC4A11, the plasma membrane protein defective in corneal dystrophies publication-title: Biochemistry doi: 10.1021/bi101887z contributor: fullname: Vilas – volume: 16 start-page: 331 year: 2004 ident: ref_19 article-title: NaBC1 is a ubiquitous electrogenic Na+ -coupled borate transporter essential for cellular boron homeostasis and cell growth and proliferation publication-title: Mol. Cell doi: 10.1016/j.molcel.2004.09.030 contributor: fullname: Park – volume: 62 start-page: 28 year: 2021 ident: ref_52 article-title: Inducible SLC4A11 Knockout Triggers Corneal Edema Through Perturbation of Corneal Endothelial Pump publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.62.7.28 contributor: fullname: Ogando – volume: 308 start-page: C176 year: 2015 ident: ref_16 article-title: Human SLC4A11-C functions as a DIDS-stimulatable H+(OH−) permeation pathway: Partial correction of R109H mutant transport publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00271.2014 contributor: fullname: Kao – volume: 54 start-page: 4330 year: 2013 ident: ref_10 article-title: Ion transport function of SLC4A11 in corneal endothelium publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.13-11929 contributor: fullname: Jalimarada – volume: 116 start-page: 1375 year: 2017 ident: ref_69 article-title: Hopefully devoted to Q: Targeting glutamine addiction in cancer publication-title: Br. J. Cancer doi: 10.1038/bjc.2017.113 contributor: fullname: Still – volume: 106 start-page: 1629 year: 2011 ident: ref_61 article-title: 3-nitro-tyrosine as a peripheral biomarker of minimal hepatic encephalopathy in patients with liver cirrhosis publication-title: Am. J. Gastroenterol. doi: 10.1038/ajg.2011.123 contributor: fullname: Montoliu – volume: 50 start-page: 4142 year: 2009 ident: ref_26 article-title: Mutational spectrum of SLC4A11 in autosomal recessive CHED in Saudi Arabia publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.08-3006 contributor: fullname: Aldahmesh – volume: 311 start-page: C945 year: 2016 ident: ref_54 article-title: Mouse SLC4A11 expressed in Xenopus oocytes is an ideally selective H+/OH− conductance pathway that is stimulated by rises in intracellular and extracellular pH publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00259.2016 contributor: fullname: Myers – volume: 34 start-page: 159 year: 2013 ident: ref_5 article-title: The SLC4 family of bicarbonate (HCO3−) transporters publication-title: Mol. Asp. Med. doi: 10.1016/j.mam.2012.10.008 contributor: fullname: Romero – volume: 13 start-page: 1327 year: 2007 ident: ref_23 article-title: Mutational spectrum of the SLC4A11 gene in autosomal recessive congenital hereditary endothelial dystrophy publication-title: Mol. Vis. contributor: fullname: Sultana – volume: 56 start-page: 7739 year: 2015 ident: ref_57 article-title: High Throughput Assay Identifies Glafenine as a Corrector for the Folding Defect in Corneal Dystrophy-Causing Mutants of SLC4A11 publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.15-17802 contributor: fullname: Chiu – volume: 318 start-page: C392 year: 2020 ident: ref_9 article-title: SLC4A11 function: Evidence for H+(OH−) and NH3-H+ transport publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00425.2019 contributor: fullname: Kao – volume: 305 start-page: C716 year: 2013 ident: ref_12 article-title: SLC4A11 is an EIPA-sensitive Na+ permeable pHi regulator publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00056.2013 contributor: fullname: Ogando – volume: 294 start-page: 20135 year: 2019 ident: ref_59 article-title: Monocarboxylate transporter 4 (MCT4) is a high affinity transporter capable of exporting lactate in high-lactate microenvironments publication-title: J. Biol. Chem. doi: 10.1074/jbc.RA119.009093 contributor: fullname: Sandoval – volume: 61 start-page: 7 year: 2020 ident: ref_50 article-title: Corneal Endothelial Pump Coupling to Lactic Acid Efflux in the Rabbit and Mouse publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.61.2.7 contributor: fullname: Li – volume: 17 start-page: 656 year: 2008 ident: ref_13 article-title: SLC4A11 mutations in Fuchs endothelial corneal dystrophy publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddm337 contributor: fullname: Vithana – volume: 293 start-page: R2136 year: 2007 ident: ref_4 article-title: Molecular expression of SLC4-derived Na+-dependent anion transporters in selected human tissues publication-title: Am. J. Physiol. Regul. Integr. Comp. Physiol. doi: 10.1152/ajpregu.00356.2007 contributor: fullname: Damkier – volume: 22 start-page: 4579 year: 2013 ident: ref_15 article-title: Transmembrane water-flux through SLC4A11: A route defective in genetic corneal diseases publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddt307 contributor: fullname: Vilas – volume: 311 start-page: C942 year: 2016 ident: ref_58 article-title: H(OH), H(OH), H(OH): A holiday perspective. Focus on “Mouse SLC4A11 expressed in Xenopus oocytes is an ideally selective H+/OH− conductance pathway that is stimulated by rises in intracellular and extracellular Ph” publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00309.2016 contributor: fullname: Nehrke – volume: 311 start-page: C735 year: 2016 ident: ref_11 article-title: Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00078.2016 contributor: fullname: Loganathan – volume: 31 start-page: 1261 year: 2010 ident: ref_39 article-title: Missense mutations in the sodium borate cotransporter SLC4A11 cause late-onset Fuchs corneal dystrophy publication-title: Hum. Mutat. doi: 10.1002/humu.21356 contributor: fullname: Riazuddin – volume: 35 start-page: 1082 year: 2014 ident: ref_40 article-title: Corneal dystrophy-causing SLC4A11 mutants: Suitability for folding-correction therapy publication-title: Hum. Mutat. doi: 10.1002/humu.22601 contributor: fullname: Loganathan – volume: 29 start-page: 41 year: 2008 ident: ref_24 article-title: Mutation in the SLC4A11 gene associated with autosomal recessive congenital hereditary endothelial dystrophy in a large Saudi family publication-title: Ophthalmic Genet. doi: 10.1080/13816810701850033 contributor: fullname: Shah – volume: 39 start-page: 676 year: 2018 ident: ref_41 article-title: Molecular phenotype of SLC4A11 missense mutants: Setting the stage for personalized medicine in corneal dystrophies publication-title: Hum. Mutat. doi: 10.1002/humu.23401 contributor: fullname: Alka – volume: 34 start-page: 668 year: 2015 ident: ref_65 article-title: Mutations in the Corneal Endothelial Dystrophy-Associated Gene SLC4A11 Render the Cells More Vulnerable to Oxidative Insults publication-title: Cornea doi: 10.1097/ICO.0000000000000421 contributor: fullname: Roy – volume: 311 start-page: C820 year: 2016 ident: ref_3 article-title: Multifunctional Ion Transport Properties of Human SLC4A11: Comparison of the SLC4A11-B and SLC4A11-C Variants publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00233.2016 contributor: fullname: Kao – volume: 481 start-page: 385 year: 2011 ident: ref_60 article-title: Reductive carboxylation supports growth in tumour cells with defective mitochondria publication-title: Nature doi: 10.1038/nature10642 contributor: fullname: Mullen – volume: 180 start-page: 86 year: 2019 ident: ref_43 article-title: R125H, W240S, C386R, and V507I SLC4A11 mutations associated with corneal endothelial dystrophy affect the transporter function but not trafficking in PS120 cells publication-title: Exp. Eye Res. doi: 10.1016/j.exer.2018.12.003 contributor: fullname: Li – volume: 51 start-page: 1106 year: 2011 ident: ref_63 article-title: Uncoupling proteins and the control of mitochondrial reactive oxygen species production publication-title: Free Radic Biol. Med. doi: 10.1016/j.freeradbiomed.2011.06.022 contributor: fullname: Mailloux – volume: 44 start-page: 64 year: 2007 ident: ref_8 article-title: Autosomal recessive corneal endothelial dystrophy (CHED2) is associated with mutations in SLC4A11 publication-title: J. Med. Genet. doi: 10.1136/jmg.2006.044644 contributor: fullname: Jiao – volume: 61 start-page: 39 year: 2020 ident: ref_44 article-title: Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.61.8.39 contributor: fullname: Zhang – volume: 38 start-page: 755 year: 2006 ident: ref_21 article-title: Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2) publication-title: Nat. Genet. doi: 10.1038/ng1824 contributor: fullname: Vithana – volume: 26 start-page: 101260 year: 2019 ident: ref_46 article-title: Ammonia sensitive SLC4A11 mitochondrial uncoupling reduces glutamine induced oxidative stress publication-title: Redox Biol. doi: 10.1016/j.redox.2019.101260 contributor: fullname: Ogando – volume: 62 start-page: 15 year: 2021 ident: ref_47 article-title: Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.62.12.15 contributor: fullname: Shyam – volume: 311 start-page: C116 year: 2016 ident: ref_49 article-title: Fluid transport by the cornea endothelium is dependent on buffering lactic acid efflux publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00095.2016 contributor: fullname: Li – volume: 177 start-page: 2278 year: 2010 ident: ref_29 article-title: Evidence of oxidative stress in the pathogenesis of fuchs endothelial corneal dystrophy publication-title: Am. J. Pathol. doi: 10.2353/ajpath.2010.100279 contributor: fullname: Jurkunas – ident: ref_6 doi: 10.1371/journal.pone.0187385 – ident: ref_55 doi: 10.1007/s00709-021-01677-3 – volume: 594 start-page: 7341 year: 2016 ident: ref_64 article-title: Hyperammonaemia-induced skeletal muscle mitochondrial dysfunction results in cataplerosis and oxidative stress publication-title: J. Physiol. doi: 10.1113/JP272796 contributor: fullname: Davuluri – volume: 282 start-page: 1103 year: 2001 ident: ref_1 article-title: Human BTR1, a new bicarbonate transporter superfamily member and human AE4 from kidney publication-title: Biochem. Biophys. Res. Commun. doi: 10.1006/bbrc.2001.4692 contributor: fullname: Parker – volume: 7 start-page: 4074 year: 2017 ident: ref_27 article-title: SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stress publication-title: Sci. Rep. doi: 10.1038/s41598-017-03654-4 contributor: fullname: Guha – volume: 27 start-page: 4044 year: 2020 ident: ref_70 article-title: Clinical Significance of a Gene Signature Generated from Tumor Budding Grade in Colon Cancer publication-title: Ann. Surg. Oncol. doi: 10.1245/s10434-020-08498-3 contributor: fullname: Shinto – volume: 214 start-page: 108884 year: 2021 ident: ref_51 article-title: RNA sequencing uncovers alterations in corneal endothelial metabolism, pump and barrier functions of SLC4A11 KO mice publication-title: Exp. Eye Res. doi: 10.1016/j.exer.2021.108884 contributor: fullname: Ogando – volume: 285 start-page: 14467 year: 2010 ident: ref_32 article-title: SLC4A11 prevents osmotic imbalance leading to corneal endothelial dystrophy, deafness, and polyuria publication-title: J. Biol. Chem. doi: 10.1074/jbc.M109.094680 contributor: fullname: Groger – volume: 33 start-page: 419 year: 2012 ident: ref_17 article-title: Oligomerization of SLC4A11 protein and the severity of FECD and CHED2 corneal dystrophies caused by SLC4A11 mutations publication-title: Hum. Mutat. doi: 10.1002/humu.21655 contributor: fullname: Vilas – volume: 126 start-page: 700 year: 2008 ident: ref_25 article-title: Identification of mutations in the SLC4A11 gene in patients with recessive congenital hereditary endothelial dystrophy publication-title: Arch. Ophthalmol. doi: 10.1001/archopht.126.5.700 contributor: fullname: Hemadevi – volume: 290 start-page: 16894 year: 2015 ident: ref_53 article-title: Human SLC4A11 Is a Novel NH3/H+ Co-transporter publication-title: J. Biol. Chem. doi: 10.1074/jbc.M114.627455 contributor: fullname: Zhang – volume: 310 start-page: C161 year: 2016 ident: ref_14 article-title: The cytoplasmic domain is essential for transport function of the integral membrane transport protein SLC4A11 publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00246.2015 contributor: fullname: Loganathan – volume: 59 start-page: 4258 year: 2018 ident: ref_42 article-title: Ophthalmic Nonsteroidal Anti-Inflammatory Drugs as a Therapy for Corneal Dystrophies Caused by SLC4A11 Mutation publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.18-24301 contributor: fullname: Alka – volume: 26 start-page: 896 year: 2007 ident: ref_22 article-title: Autosomal recessive CHED associated with novel compound heterozygous mutations in SLC4A11 publication-title: Cornea doi: 10.1097/ICO.0b013e318074bb01 contributor: fullname: Aldave – volume: 62 start-page: 4 year: 2021 ident: ref_37 article-title: Mitochondrial Targeting of the Ammonia-Sensitive Uncoupler SLC4A11 by the Chaperone-Mediated Carrier Pathway in Corneal Endothelium publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.62.12.4 contributor: fullname: Choi – volume: 7 start-page: e14232 year: 2019 ident: ref_38 article-title: SLC4A11 disruption causes duct cell loss and impairs NaCl reabsorption in female mouse submandibular glands publication-title: Physiol. Rep. doi: 10.14814/phy2.14232 contributor: fullname: Yang – volume: 4 start-page: 24 year: 2005 ident: ref_18 article-title: Borate transport and cell growth and proliferation. Not only in plants publication-title: Cell Cycle doi: 10.4161/cc.4.1.1394 contributor: fullname: Park – volume: 33 start-page: 247 year: 2014 ident: ref_33 article-title: Congenital hereditary endothelial dystrophy caused by SLC4A11 mutations progresses to Harboyan syndrome publication-title: Cornea doi: 10.1097/ICO.0000000000000041 contributor: fullname: Siddiqui – volume: 123 start-page: 3678 year: 2013 ident: ref_68 article-title: Glutamine and cancer: Cell biology, physiology, and clinical opportunities publication-title: J. Clin. Investig. doi: 10.1172/JCI69600 contributor: fullname: Hensley – volume: 16 start-page: 619 year: 2016 ident: ref_67 article-title: From Krebs to clinic: Glutamine metabolism to cancer therapy publication-title: Nat. Rev. Cancer doi: 10.1038/nrc.2016.71 contributor: fullname: Altman – volume: 16 start-page: 292 year: 2017 ident: ref_45 article-title: Glutaminolysis is Essential for Energy Production and Ion Transport in Human Corneal Endothelium publication-title: EBioMedicine doi: 10.1016/j.ebiom.2017.01.004 contributor: fullname: Zhang – volume: 3 start-page: 28 year: 2008 ident: ref_30 article-title: Congenital hereditary endothelial dystrophy with progressive sensorineural deafness (Harboyan syndrome) publication-title: Orphanet J. Rare Dis. doi: 10.1186/1750-1172-3-28 contributor: fullname: Desir – volume: 54 start-page: 6179 year: 2013 ident: ref_35 article-title: Mice with a targeted disruption of SLC4A11 model the progressive corneal changes of congenital hereditary endothelial dystrophy publication-title: Investig. Ophthalmol. Vis. Sci. doi: 10.1167/iovs.13-12089 contributor: fullname: Han – volume: 284 start-page: 26882 year: 2009 ident: ref_31 article-title: SLC4A11 gene disruption in mice: Cellular targets of sensorineuronal abnormalities publication-title: J. Biol. Chem. doi: 10.1074/jbc.M109.008102 contributor: fullname: Lopez – volume: 430 start-page: 3873 year: 2018 ident: ref_62 article-title: Use the Protonmotive Force: Mitochondrial Uncoupling and Reactive Oxygen Species publication-title: J. Mol. Biol. doi: 10.1016/j.jmb.2018.03.025 contributor: fullname: Berry – volume: 167 start-page: 299 year: 2021 ident: ref_66 article-title: Enhanced expression of SLC4A11 by tert-Butylhydroquinone is mediated by direct binding of Nrf2 to the promoter of SLC4A11 publication-title: Free Radic Biol. Med. doi: 10.1016/j.freeradbiomed.2021.03.006 contributor: fullname: Guha – ident: ref_7 doi: 10.3390/jcm10091979 – volume: 39 start-page: 354 year: 2020 ident: ref_34 article-title: Coexistence of Congenital Hereditary Endothelial Dystrophy and Fuchs Endothelial Corneal Dystrophy Associated With SLC4A11 Mutations in Affected Families publication-title: Cornea doi: 10.1097/ICO.0000000000002183 contributor: fullname: Chaurasia |
| SSID | ssj0000816105 |
| Score | 2.311743 |
| SecondaryResourceType | review_article |
| Snippet | Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H
transporter activated by NH
and alkaline pH.... Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H+ transporter activated by NH3 and alkaline pH.... Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H + transporter activated by NH 3 and alkaline pH.... |
| SourceID | doaj pubmedcentral proquest crossref pubmed |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database |
| StartPage | 197 |
| SubjectTerms | Amino acids Ammonia Animals Anion Transport Proteins - genetics Anion Transport Proteins - metabolism Antioxidants Autophagy Bicarbonates Cochlea Cornea corneal endothelial dystrophy Dystrophy Edema Endothelium Gene Expression Regulation Genetic Predisposition to Disease Glutamine Humans Hydrogen Hyperpolarization Kidneys lactate Localization Lysosomes MCT4 Membrane potential Mitochondria Mitochondria - metabolism Mutation Oxidative metabolism Oxidative stress Oxidative Stress - genetics Physiology Plasma Polyuria Proteins Protons Review Salivary gland Stem cells |
| SummonAdditionalLinks | – databaseName: Directory of Open Access Journals dbid: DOA link: http://sdu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3dSxwxEA9WEPpS6kfbsyoRii92cTcfm8Q3P7kHreAp9KlLNh96oLni3UH9753ZPc87Efri6yYks_PLZGZC5hdCfuReelsEn8USj260Mpk1PGYenEeQSEWpsRq521O_fuvjE6TJmT71hXfCWnrgVnF7vLDSeeFZabTQPNjAtbCQD9YQG2jb8nzmeiaZavZgDZFMLltSTQ55_R6egw_B14HDQ4KnGSfUcPW_FWC-vic543hOP5NPk4iRHrSSLpOFkFbIUvuG5OMq-QNA0-4ufWEpf6C9syNxUBT79BLpmmg_0fMwArTv-sP7n_TiX983dN-01xSKUJs8PQfLhp0weVyQ9Dq5wRhrdW_WyNXpydVRN5s8mpA5KdQoc4VxNkimYq0YlkYHbQJjBpxQNMJYq2ofo2ARjNEKo6Ebl8J7XmNRa86_kMU0SOEbobk2zsSidDF3guVO104UMJYu6-ghS-qQnWclVn9baowKUgrUdjWn7Q45RBVPOyGjdfMBcK4mOFf_w7lDNp4BqiZmNqxYiQT1QinZIdvTZjAQnN-mMBg3fRj4YF2CHF9bPKeScImlyAUMruaQnhN1viX1bxsSbq0UF6Vcf49_-04-MqyqwJMdtUEWRw_jsEk-DP14q1nWT6Ch_IM priority: 102 providerName: Directory of Open Access Journals |
| Title | The H + Transporter SLC4A11: Roles in Metabolism, Oxidative Stress and Mitochondrial Uncoupling |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/35053313 https://www.proquest.com/docview/2621274775 https://search.proquest.com/docview/2622284867 https://pubmed.ncbi.nlm.nih.gov/PMC8773465 https://doaj.org/article/31a5cd4d2698483eae384aeb2b9518a3 |
| Volume | 11 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://sdu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELbYSkhcEG8CbWUkxAXSTWI7trm121Z7YAGxReJE5PjRRup6q31I8O8ZO8nSoJ64xk4ymofnoZnPCL3NDDMqtyZ1ZSjdCC5TJYlLDTgPywIUpQjTyNM5__xDnJ4FmBzWz8LEpn1dN0f-enHkm6vYW3mz0OO-T2z8dTYRnBNasvEIjSA2vJWix-NXQBCTsRZPk0BKPw4l8DW4OfB1Mly6R1gYQM3JwBVFxP67wsx_uyVvuZ_zR-hhFzfi45a-x-ie9U_Q_fYmyd9P0U8QN56-x3-xyld4_mlCj_P8I_4WQJtw4_HMbkDm18168QF_-dWYCPqN53FcBCtv8AzsG85Db4Ja4u9eL7dhYvfyGbo4P7uYTNPu6oRUM8o3qc6lVpYV3NW8CAPSVkhbFBJckZNUKsVr4xwtHJikolLANsKoMaQOo60ZeY72_NLblwhnQmrp8lK7TNMi06LWNIdvibJ2BnKlBL3rmVjdtAAZFSQWgfHVgPEJOgks3m0KuNbxwXJ1WXXSrUiumDbUABGCCmKVJYIqyP5riASFIgna7wVUdca2rooywNRTzlmC3uyWwUzC_5W3y23cU4AnFiXQ8aKV546SXh8SxAeSHpA6XAHNjFDcnSa--u83X6MHRRioCEUdvo_2NqutPUCjtdkexvLAYVTuP9Be_eE |
| link.rule.ids | 230,315,729,782,786,866,887,2108,27935,27936,53803,53805 |
| linkProvider | National Library of Medicine |
| linkToHtml | http://sdu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELZoEYILb2iggJEQF0g38SO2uZWl1SJ2C2IXqScix3baSN1stQ8J_j1jJ1kaxKnX2ElGnm88M9bMZ4TeJJZbnTobl5k_upFCxVrRMrbgPBz3VJTSdyOPpuLkVH468jQ5vOuFCUX7pqgO6ov5QV2dh9rKy7kZdHVig2-ToRSCsowPdtBNsNeEXknSwwYsIYxJeMOoSSGpH_hD8BU4OvB2yl-7R7lvQU1pzxkFzv7_BZr_1ktecUDH964p-n10t4048WEz_ADdcPVDdKu5g_L3I_QTgIJH7_BflvMlno6H7DBNP-Dvnu4JVzWeuDWg5aJazd_jr78qG-jC8TQ0mmBdWzyBnQF20tp6QOMftVlsfK_v2WM0Oz6aDUdxe-lCbDgT69ikymjHiSgLQXxrtZPKEaLAiZWKKa1FYcuSkRKMWTMlYRrlzFpa-KbYhD5Bu_WidnsIJ1IZVaaZKRPDSGJkYVgK35JZUVrIsiL0tlv8_LKh1sghJfEKy3sKi9BHr5rtJM-IHR4slmd5u7g5TTU3llkQQjJJnXZUMu0KUkAMKTWN0H6n2Lw101VOMk9wz4TgEXq9HQYD8__XtVtswhwCPlxmIMfTBgdbSTocRUj0ENITtT8CwAgk3i0Qnl37zVfo9mg2GefjzydfnqM7xLdl-KMhsY9218uNe4F2VnbzMpjGH-6cEo4 |
| linkToPdf | http://sdu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwELZoEYgL70eggJEQF0jzsB3b3Mq2q0V0S8UWqScix48Sqetd7UOCf884yS4N4gTXZJKMMt94xtbMNwi9Tg0zKrMmdkU4uhFcxkoSFxsIHpYFKkoRupFHE35yLg6PAk3OdtRXU7Svq3rfX073ff29qa2cT3WyqRNLTscDwTmhBUvmxiU76Dr4bMqubNSbRVhAKpOyllWTwMY-CQfhSwh2EPFkGL1HWGhDzUgvIDW8_X9LNv-smbwShIZ3_kP9u-h2l3nig1bkHrpm_X10o51F-fMB-gaAwaO3-Dfb-QJPjgf0IMve4y-B9gnXHo_tClBzWS-n7_DnH7VpaMPxpGk4wcobPIYVAlZUbwKw8VevZ-vQ83vxEJ0Nj84Go7gbvhBrRvkq1pnUyrKcu4rnocXaCmnzXEIwc5JKpXhlnKO5A6dWVAoQI4waQ6rQHJuSR2jXz7x9gnAqpJYuK7RLNc1TLSpNM3iXKCpnYLcVoTcbA5TzlmKjhK1JMFrZM1qEPgTzbIUCM3ZzYba4KLsfXJJMMW2oASUEFcQqSwRVtsoryCWFIhHa2xi37Nx1WeZFILqnnLMIvdreBkcL31feztaNTA6xXBSgx-MWC1tNNliKEO-hpKdq_w6AoyHz7sDw9J-ffIlunh4Oy-OPJ5-eoVt56M4IJ0R8D-2uFmv7HO0szfpF4x2_AJZsFQ4 |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+H%2B+Transporter+SLC4A11%3A+Roles+in+Metabolism%2C+Oxidative+Stress+and+Mitochondrial+Uncoupling&rft.jtitle=Cells+%28Basel%2C+Switzerland%29&rft.au=Bonanno%2C+Joseph+A&rft.au=Raji+Shyam&rft.au=Choi%2C+Moonjung&rft.au=Ogando%2C+Diego+G&rft.date=2022-01-07&rft.pub=MDPI+AG&rft.eissn=2073-4409&rft.volume=11&rft.issue=2&rft.spage=197&rft_id=info:doi/10.3390%2Fcells11020197&rft.externalDBID=HAS_PDF_LINK |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2073-4409&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2073-4409&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2073-4409&client=summon |