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{{Infobox_gene}}
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'''Krueppel-like factor 11''' is a [[protein]] that in humans is encoded by the ''KLF11'' [[gene]].<ref name="pmid9748269">{{cite journal | vauthors = Cook T, Gebelein B, Mesa K, Mladek A, Urrutia R | title = Molecular cloning and characterization of TIEG2 reveals a new subfamily of transforming growth factor-beta-inducible Sp1-like zinc finger-encoding genes involved in the regulation of cell growth | journal = The Journal of Biological Chemistry | volume = 273 | issue = 40 | pages = 25929–36 | date = Oct 1998 | pmid = 9748269 | pmc =  | doi = 10.1074/jbc.273.40.25929 }}</ref><ref name="pmid11087666">{{cite journal | vauthors = Scohy S, Gabant P, Van Reeth T, Hertveldt V, Drèze PL, Van Vooren P, Rivière M, Szpirer J, Szpirer C | title = Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family | journal = Genomics | volume = 70 | issue = 1 | pages = 93–101 | date = Nov 2000 | pmid = 11087666 | pmc = | doi = 10.1006/geno.2000.6362 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: KLF11 Kruppel-like factor 11| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=8462| accessdate = }}</ref>
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<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot. See Template:PBB_Controls to Stop updates. -->
KLF11 is a mesoderm derived, [[zinc finger transcription factor]] in the [[Kruppel-like factors|Krüppel-like factor]] (KLF) family. It binds to SP1- like GC- rich sequences in epsilon and gamma globin [[Promoter (genetics)|gene promoters]] inhibiting cellular growth and causing apoptosis. In the regulation of genes, it is involved in cellular inflammation and differentiation, making it an essential factor in early embryonic development. This transcription factor binds to promoters of genes involved in cholesterol, prostaglandin, neurotransmitter, fat, and sugar metabolism, specifically pancreatic beta cell function. Defects in KLF11 affect glucose metabolism, insulin transcription, insulin processing, and insulin secretion which cause type 2 diabetes in adults and [[Maturity onset diabetes of the young|maturity-onset diabetes of the young]] type 7. These types of diabetes are caused by KLF11 interacting with [[Corepressor|co-repressors]] in the pancreatic islet beta cells. KLF11 has recently been shown to be involved in [[endometriosis]] since it regulated the expression of extracellular matrix genes. Its absence in extracellular matrix genes created a more fibrogenic response by the tissue. This was proved by creating a “knockout” model. The experiment showed that the absence of KLF11 showed higher amounts of fibrosis indicating that it prevents the growth of endometriotic lesions and inhibits pathological scarring.
{{GNF_Protein_box
| image = 
| image_source = 
| PDB =
| Name = Kruppel-like factor 11
| HGNCid = 11811
| Symbol = KLF11
| AltSymbols =; FKLF; FKLF1; MODY7; TIEG2; Tieg3
| OMIM = 603301
| ECnumber = 
| Homologene = 2668
| MGIid = 2653368
| GeneAtlas_image1 = PBB_GE_KLF11_218486_at_tn.png
| Function = {{GNF_GO|id=GO:0003676 |text = nucleic acid binding}} {{GNF_GO|id=GO:0003700 |text = transcription factor activity}} {{GNF_GO|id=GO:0008270 |text = zinc ion binding}} {{GNF_GO|id=GO:0046872 |text = metal ion binding}}
| Component = {{GNF_GO|id=GO:0005622 |text = intracellular}} {{GNF_GO|id=GO:0005634 |text = nucleus}}
| Process = {{GNF_GO|id=GO:0000122 |text = negative regulation of transcription from RNA polymerase II promoter}} {{GNF_GO|id=GO:0006350 |text = transcription}} {{GNF_GO|id=GO:0006366 |text = transcription from RNA polymerase II promoter}} {{GNF_GO|id=GO:0008285 |text = negative regulation of cell proliferation}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 8462
    | Hs_Ensembl = ENSG00000172059
    | Hs_RefseqProtein = XP_001129527
    | Hs_RefseqmRNA = XM_001129527
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 2
    | Hs_GenLoc_start = 10101133
    | Hs_GenLoc_end = 10112414
    | Hs_Uniprot = O14901
    | Mm_EntrezGene = 194655
    | Mm_Ensembl = ENSMUSG00000020653
    | Mm_RefseqmRNA = NM_178357
    | Mm_RefseqProtein = NP_848134
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 12
    | Mm_GenLoc_start = 25240450
    | Mm_GenLoc_end = 25251853
    | Mm_Uniprot = Q8BHJ1
  }}
}}
'''Kruppel-like factor 11''', also known as '''KLF11''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: KLF11 Kruppel-like factor 11| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=8462| accessdate = }}</ref>


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot. See Template:PBB_Controls to Stop updates. -->
<ref name="Daftary_2013">{{cite journal | vauthors = Daftary GS, Zheng Y, Tabbaa ZM, Schoolmeester JK, Gada RP, Grzenda AL, Mathison AJ, Keeney GL, Lomberk GA, Urrutia R | title = A novel role of the Sp/KLF transcription factor KLF11 in arresting progression of endometriosis | journal = PLoS One | volume = 8 | issue = 3 | pages = e60165 | year = 2013 | pmid = 23555910 | pmc = 3610699 | doi = 10.1371/journal.pone.0060165 }}</ref><ref name="Mathison_2013">{{cite journal | vauthors = Mathison A, Grzenda A, Lomberk G, Velez G, Buttar N, Tietz P, Hendrickson H, Liebl A, Xiong YY, Gores G, Fernandez-Zapico M, Larusso NF, Faubion W, Shah VH, Urrutia R | title = Role for Krüppel-like transcription factor 11 in mesenchymal cell function and fibrosis | journal = PLoS One | volume = 8 | issue = 9 | pages = e75311 | year = 2013 | pmid = 24069400 | pmc = 3775729 | doi = 10.1371/journal.pone.0075311 }}</ref><ref name="Spittau_2012">{{cite journal | vauthors = Spittau B, Krieglstein K | title = Klf10 and Klf11 as mediators of TGF-beta superfamily signaling | journal = Cell and Tissue Research | volume = 347 | issue = 1 | pages = 65–72 | year = 2012 | pmid = 21574058 | doi = 10.1007/s00441-011-1186-6 }}</ref>
{{PBB_Summary
| section_title =  
| summary_text =  
}}


==See also==
== Interactions ==
* [[Kruppel-like factors]]


==References==
KLF11 has been shown to [[Protein-protein interaction|interact]] with [[SIN3A]].<ref name=pmid11438660>{{cite journal | vauthors = Zhang JS, Moncrieffe MC, Kaczynski J, Ellenrieder V, Prendergast FG, Urrutia R | title = A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A | journal = Molecular and Cellular Biology | volume = 21 | issue = 15 | pages = 5041–9 | date = Aug 2001 | pmid = 11438660 | pmc = 87230 | doi = 10.1128/MCB.21.15.5041-5049.2001 }}</ref><ref name=pmid12006497>{{cite journal | vauthors = Ellenrieder V, Zhang JS, Kaczynski J, Urrutia R | title = Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor | journal = The EMBO Journal | volume = 21 | issue = 10 | pages = 2451–60 | date = May 2002 | pmid = 12006497 | pmc = 126002 | doi = 10.1093/emboj/21.10.2451 }}</ref>
{{reflist|2}}


==Further reading==
== See also ==
* [[Kruppel-like factors|Krüppel-like factors]]
* [[Maturity onset diabetes of the young]]
 
== References ==
{{reflist}}
 
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
* {{cite journal | vauthors = Asano H, Li XS, Stamatoyannopoulos G | title = FKLF, a novel Krüppel-like factor that activates human embryonic and fetal beta-like globin genes | journal = Molecular and Cellular Biology | volume = 19 | issue = 5 | pages = 3571–9 | date = May 1999 | pmid = 10207080 | pmc = 84149 | doi = }}
| citations =
* {{cite journal | vauthors = Zhang JS, Moncrieffe MC, Kaczynski J, Ellenrieder V, Prendergast FG, Urrutia R | title = A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A | journal = Molecular and Cellular Biology | volume = 21 | issue = 15 | pages = 5041–9 | date = Aug 2001 | pmid = 11438660 | pmc = 87230 | doi = 10.1128/MCB.21.15.5041-5049.2001 }}
*{{cite journal  | author=Cook T, Gebelein B, Mesa K, ''et al.'' |title=Molecular cloning and characterization of TIEG2 reveals a new subfamily of transforming growth factor-beta-inducible Sp1-like zinc finger-encoding genes involved in the regulation of cell growth. |journal=J. Biol. Chem. |volume=273 |issue= 40 |pages= 25929-36 |year= 1998 |pmid= 9748269 |doi=  }}
* {{cite journal | vauthors = Jia L, Young MF, Powell J, Yang L, Ho NC, Hotchkiss R, Robey PG, Francomano CA | title = Gene expression profile of human bone marrow stromal cells: high-throughput expressed sequence tag sequencing analysis | journal = Genomics | volume = 79 | issue = 1 | pages = 7–17 | date = Jan 2002 | pmid = 11827452 | doi = 10.1006/geno.2001.6683 }}
*{{cite journal | author=Asano H, Li XS, Stamatoyannopoulos G |title=FKLF, a novel Krüppel-like factor that activates human embryonic and fetal beta-like globin genes. |journal=Mol. Cell. Biol. |volume=19 |issue= 5 |pages= 3571-9 |year= 1999 |pmid= 10207080 |doi= }}
* {{cite journal | vauthors = Ellenrieder V, Zhang JS, Kaczynski J, Urrutia R | title = Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor | journal = The EMBO Journal | volume = 21 | issue = 10 | pages = 2451–60 | date = May 2002 | pmid = 12006497 | pmc = 126002 | doi = 10.1093/emboj/21.10.2451 }}
*{{cite journal  | author=Scohy S, Gabant P, Van Reeth T, ''et al.'' |title=Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family. |journal=Genomics |volume=70 |issue= 1 |pages= 93-101 |year= 2001 |pmid= 11087666 |doi= 10.1006/geno.2000.6362 }}
* {{cite journal | vauthors = Ou XM, Chen K, Shih JC | title = Dual functions of transcription factors, transforming growth factor-beta-inducible early gene (TIEG)2 and Sp3, are mediated by CACCC element and Sp1 sites of human monoamine oxidase (MAO) B gene | journal = The Journal of Biological Chemistry | volume = 279 | issue = 20 | pages = 21021–8 | date = May 2004 | pmid = 15024015 | doi = 10.1074/jbc.M312638200 }}
*{{cite journal | author=Zhang JS, Moncrieffe MC, Kaczynski J, ''et al.'' |title=A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A. |journal=Mol. Cell. Biol. |volume=21 |issue= 15 |pages= 5041-9 |year= 2001 |pmid= 11438660 |doi= 10.1128/MCB.21.15.5041-5049.2001 }}
* {{cite journal | vauthors = Ellenrieder V, Buck A, Harth A, Jungert K, Buchholz M, Adler G, Urrutia R, Gress TM | title = KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells | journal = Gastroenterology | volume = 127 | issue = 2 | pages = 607–20 | date = Aug 2004 | pmid = 15300592 | doi = 10.1053/j.gastro.2004.05.018 }}
*{{cite journal | author=Jia L, Young MF, Powell J, ''et al.'' |title=Gene expression profile of human bone marrow stromal cells: high-throughput expressed sequence tag sequencing analysis. |journal=Genomics |volume=79 |issue= 1 |pages= 7-17 |year= 2002 |pmid= 11827452 |doi= 10.1006/geno.2001.6683 }}
* {{cite journal | vauthors = Cao S, Fernandez-Zapico ME, Jin D, Puri V, Cook TA, Lerman LO, Zhu XY, Urrutia R, Shah V | title = KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling | journal = The Journal of Biological Chemistry | volume = 280 | issue = 3 | pages = 1901–10 | date = Jan 2005 | pmid = 15531587 | doi = 10.1074/jbc.M407941200 }}
*{{cite journal | author=Ellenrieder V, Zhang JS, Kaczynski J, Urrutia R |title=Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor. |journal=EMBO J. |volume=21 |issue= 10 |pages= 2451-60 |year= 2002 |pmid= 12006497 |doi= 10.1093/emboj/21.10.2451 }}
* {{cite journal | vauthors = Neve B, Fernandez-Zapico ME, Ashkenazi-Katalan V, Dina C, Hamid YH, Joly E, Vaillant E, Benmezroua Y, Durand E, Bakaher N, Delannoy V, Vaxillaire M, Cook T, Dallinga-Thie GM, Jansen H, Charles MA, Clément K, Galan P, Hercberg S, Helbecque N, Charpentier G, Prentki M, Hansen T, Pedersen O, Urrutia R, Melloul D, Froguel P | title = Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 102 | issue = 13 | pages = 4807–12 | date = Mar 2005 | pmid = 15774581 | pmc = 554843 | doi = 10.1073/pnas.0409177102 }}
*{{cite journal | author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899-903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 }}
* {{cite journal|authorlink13=Huda Zoghbi | vauthors = Lim J, Hao T, Shaw C, Patel AJ, Szabó G, Rual JF, Fisk CJ, Li N, Smolyar A, Hill DE, Barabási AL, Vidal M, Zoghbi HY | title = A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration | journal = Cell | volume = 125 | issue = 4 | pages = 801–14 | date = May 2006 | pmid = 16713569 | doi = 10.1016/j.cell.2006.03.032 }}
*{{cite journal  | author=Ota T, Suzuki Y, Nishikawa T, ''et al.'' |title=Complete sequencing and characterization of 21,243 full-length human cDNAs. |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40-5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285 }}
* {{cite journal | vauthors = Buck A, Buchholz M, Wagner M, Adler G, Gress T, Ellenrieder V | title = The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer | journal = Molecular Cancer Research | volume = 4 | issue = 11 | pages = 861–72 | date = Nov 2006 | pmid = 17114344 | doi = 10.1158/1541-7786.MCR-06-0081 }}
*{{cite journal  | author=Ou XM, Chen K, Shih JC |title=Dual functions of transcription factors, transforming growth factor-beta-inducible early gene (TIEG)2 and Sp3, are mediated by CACCC element and Sp1 sites of human monoamine oxidase (MAO) B gene. |journal=J. Biol. Chem. |volume=279 |issue= 20 |pages= 21021-8 |year= 2004 |pmid= 15024015 |doi= 10.1074/jbc.M312638200 }}
* {{cite journal | vauthors = Florez JC, Saxena R, Winckler W, Burtt NP, Almgren P, Bengtsson Boström K, Tuomi T, Gaudet D, Ardlie KG, Daly MJ, Altshuler D, Hirschhorn JN, Groop L | title = The Krüppel-like factor 11 (KLF11) Q62R polymorphism is not associated with type 2 diabetes in 8,676 people | journal = Diabetes | volume = 55 | issue = 12 | pages = 3620–4 | date = Dec 2006 | pmid = 17130512 | doi = 10.2337/db06-0867 }}
*{{cite journal | author=Ellenrieder V, Buck A, Harth A, ''et al.'' |title=KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells. |journal=Gastroenterology |volume=127 |issue= 2 |pages= 607-20 |year= 2004 |pmid= 15300592 |doi= }}
* {{cite journal | vauthors = Spittau B, Wang Z, Boinska D, Krieglstein K | title = Functional domains of the TGF-beta-inducible transcription factor Tieg3 and detection of two putative nuclear localization signals within the zinc finger DNA-binding domain | journal = Journal of Cellular Biochemistry | volume = 101 | issue = 3 | pages = 712–22 | date = Jun 2007 | pmid = 17252542 | doi = 10.1002/jcb.21228 }}
*{{cite journal  | author=Gerhard DS, Wagner L, Feingold EA, ''et al.'' |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121-7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 }}
* {{cite journal | vauthors = Niu X, Perakakis N, Laubner K, Limbert C, Stahl T, Brendel MD, Bretzel RG, Seufert J, Päth G | title = Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells | journal = Diabetologia | volume = 50 | issue = 7 | pages = 1433–41 | date = Jul 2007 | pmid = 17479246 | doi = 10.1007/s00125-007-0667-3 }}
*{{cite journal | author=Cao S, Fernandez-Zapico ME, Jin D, ''et al.'' |title=KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling. |journal=J. Biol. Chem. |volume=280 |issue= 3 |pages= 1901-10 |year= 2005 |pmid= 15531587 |doi= 10.1074/jbc.M407941200 }}
*{{cite journal | author=Neve B, Fernandez-Zapico ME, Ashkenazi-Katalan V, ''et al.'' |title=Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=102 |issue= 13 |pages= 4807-12 |year= 2005 |pmid= 15774581 |doi= 10.1073/pnas.0409177102 }}
*{{cite journal | author=Lim J, Hao T, Shaw C, ''et al.'' |title=A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration. |journal=Cell |volume=125 |issue= 4 |pages= 801-14 |year= 2006 |pmid= 16713569 |doi= 10.1016/j.cell.2006.03.032 }}
*{{cite journal | author=Buck A, Buchholz M, Wagner M, ''et al.'' |title=The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer. |journal=Mol. Cancer Res. |volume=4 |issue= 11 |pages= 861-72 |year= 2007 |pmid= 17114344 |doi= 10.1158/1541-7786.MCR-06-0081 }}
*{{cite journal | author=Florez JC, Saxena R, Winckler W, ''et al.'' |title=The Krüppel-like factor 11 (KLF11) Q62R polymorphism is not associated with type 2 diabetes in 8,676 people. |journal=Diabetes |volume=55 |issue= 12 |pages= 3620-4 |year= 2007 |pmid= 17130512 |doi= 10.2337/db06-0867 }}
*{{cite journal | author=Spittau B, Wang Z, Boinska D, Krieglstein K |title=Functional domains of the TGF-beta-inducible transcription factor Tieg3 and detection of two putative nuclear localization signals within the zinc finger DNA-binding domain. |journal=J. Cell. Biochem. |volume=101 |issue= 3 |pages= 712-22 |year= 2007 |pmid= 17252542 |doi= 10.1002/jcb.21228 }}
*{{cite journal | author=Niu X, Perakakis N, Laubner K, ''et al.'' |title=Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells. |journal=Diabetologia |volume=50 |issue= 7 |pages= 1433-41 |year= 2007 |pmid= 17479246 |doi= 10.1007/s00125-007-0667-3 }}
}}
{{refend}}
{{refend}}


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{{Transcription factors}}
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[[Category:Transcription factors]]
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{{gene-2-stub}}

Revision as of 02:49, 26 November 2017

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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
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Wikidata
View/Edit Human

Krueppel-like factor 11 is a protein that in humans is encoded by the KLF11 gene.[1][2][3]

KLF11 is a mesoderm derived, zinc finger transcription factor in the Krüppel-like factor (KLF) family. It binds to SP1- like GC- rich sequences in epsilon and gamma globin gene promoters inhibiting cellular growth and causing apoptosis. In the regulation of genes, it is involved in cellular inflammation and differentiation, making it an essential factor in early embryonic development. This transcription factor binds to promoters of genes involved in cholesterol, prostaglandin, neurotransmitter, fat, and sugar metabolism, specifically pancreatic beta cell function. Defects in KLF11 affect glucose metabolism, insulin transcription, insulin processing, and insulin secretion which cause type 2 diabetes in adults and maturity-onset diabetes of the young type 7. These types of diabetes are caused by KLF11 interacting with co-repressors in the pancreatic islet beta cells. KLF11 has recently been shown to be involved in endometriosis since it regulated the expression of extracellular matrix genes. Its absence in extracellular matrix genes created a more fibrogenic response by the tissue. This was proved by creating a “knockout” model. The experiment showed that the absence of KLF11 showed higher amounts of fibrosis indicating that it prevents the growth of endometriotic lesions and inhibits pathological scarring.

[4][5][6]

Interactions

KLF11 has been shown to interact with SIN3A.[7][8]

See also

References

  1. ↑ Cook T, Gebelein B, Mesa K, Mladek A, Urrutia R (Oct 1998). "Molecular cloning and characterization of TIEG2 reveals a new subfamily of transforming growth factor-beta-inducible Sp1-like zinc finger-encoding genes involved in the regulation of cell growth". The Journal of Biological Chemistry. 273 (40): 25929–36. doi:10.1074/jbc.273.40.25929. PMID 9748269.
  2. ↑ Scohy S, Gabant P, Van Reeth T, Hertveldt V, Drèze PL, Van Vooren P, Rivière M, Szpirer J, Szpirer C (Nov 2000). "Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family". Genomics. 70 (1): 93–101. doi:10.1006/geno.2000.6362. PMID 11087666.
  3. ↑ "Entrez Gene: KLF11 Kruppel-like factor 11".
  4. ↑ Daftary GS, Zheng Y, Tabbaa ZM, Schoolmeester JK, Gada RP, Grzenda AL, Mathison AJ, Keeney GL, Lomberk GA, Urrutia R (2013). "A novel role of the Sp/KLF transcription factor KLF11 in arresting progression of endometriosis". PLoS One. 8 (3): e60165. doi:10.1371/journal.pone.0060165. PMC 3610699. PMID 23555910.
  5. ↑ Mathison A, Grzenda A, Lomberk G, Velez G, Buttar N, Tietz P, Hendrickson H, Liebl A, Xiong YY, Gores G, Fernandez-Zapico M, Larusso NF, Faubion W, Shah VH, Urrutia R (2013). "Role for Krüppel-like transcription factor 11 in mesenchymal cell function and fibrosis". PLoS One. 8 (9): e75311. doi:10.1371/journal.pone.0075311. PMC 3775729. PMID 24069400.
  6. ↑ Spittau B, Krieglstein K (2012). "Klf10 and Klf11 as mediators of TGF-beta superfamily signaling". Cell and Tissue Research. 347 (1): 65–72. doi:10.1007/s00441-011-1186-6. PMID 21574058.
  7. ↑ Zhang JS, Moncrieffe MC, Kaczynski J, Ellenrieder V, Prendergast FG, Urrutia R (Aug 2001). "A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A". Molecular and Cellular Biology. 21 (15): 5041–9. doi:10.1128/MCB.21.15.5041-5049.2001. PMC 87230. PMID 11438660.
  8. ↑ Ellenrieder V, Zhang JS, Kaczynski J, Urrutia R (May 2002). "Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor". The EMBO Journal. 21 (10): 2451–60. doi:10.1093/emboj/21.10.2451. PMC 126002. PMID 12006497.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.



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