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Recent research has demonstrated alteration in PKMζ in [[Alzheimer's disease]] (''see [[Long-term potentiation#Alzheimer's disease|Long-term potentiation]]''), providing a potential link between this kinase and neurodegeneration.<ref name="pmid16691113">{{cite journal |author=Crary JF, Shao CY, Mirra SS, Hernandez AI, Sacktor TC |title=Atypical protein kinase C in neurodegenerative disease I: PKMzeta aggregates with limbic neurofibrillary tangles and AMPA receptors in Alzheimer disease |journal=J. Neuropathol. Exp. Neurol. |volume=65 |issue=4 |pages=319–26 |year=2006 |month=April |pmid=16691113 |doi=10.1097/01.jnen.0000218442.07664.04 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00005072-200604000-00002}}</ref>
Recent research has demonstrated alteration in PKMζ in [[Alzheimer's disease]] (''see [[Long-term potentiation#Alzheimer's disease|Long-term potentiation]]''), providing a potential link between this kinase and neurodegeneration.<ref name="pmid16691113">{{cite journal |author=Crary JF, Shao CY, Mirra SS, Hernandez AI, Sacktor TC |title=Atypical protein kinase C in neurodegenerative disease I: PKMzeta aggregates with limbic neurofibrillary tangles and AMPA receptors in Alzheimer disease |journal=J. Neuropathol. Exp. Neurol. |volume=65 |issue=4 |pages=319–26 |year=2006 |month=April |pmid=16691113 |doi=10.1097/01.jnen.0000218442.07664.04 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00005072-200604000-00002}}</ref>

==Model organisms==
{| class="wikitable sortable collapsible collapsed" border="1" cellpadding="2" style="float: right;" |
|+ ''Prkcz'' knockout mouse phenotype
|-
! Characteristic!! Phenotype

|-
| [[Homozygote]] viability || bgcolor="#488ED3"|Normal
|-
| Fertility || bgcolor="#488ED3"|Normal
|-
| Body weight || bgcolor="#488ED3"|Normal
|-
| [[Open_Field_(animal_test)|Anxiety]] || bgcolor="#488ED3"|Normal
|-
| Neurological assessment || bgcolor="#488ED3"|Normal
|-
| Grip strength || bgcolor="#488ED3"|Normal
|-
| [[Hot_plate_test|Hot plate]] || bgcolor="#488ED3"|Normal
|-
| [[Dysmorphology]] || bgcolor="#488ED3"|Normal
|-
| [[Indirect calorimetry]] || bgcolor="#488ED3"|Normal
|-
| [[Glucose tolerance test]] || bgcolor="#488ED3"|Normal
|-
| [[Auditory brainstem response]] || bgcolor="#488ED3"|Normal
|-
| [[Dual-energy_X-ray_absorptiometry|DEXA]] || bgcolor="#488ED3"|Normal
|-
| [[Radiography]] || bgcolor="#488ED3"|Normal
|-
| Body temperature || bgcolor="#488ED3"|Normal
|-
| Eye morphology || bgcolor="#C40000"|Abnormal<ref name="Eye morphology">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBGK/eye-morphology/ |title=Eye morphology data for Prkcz |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| [[Clinical chemistry]] || bgcolor="#C40000"|Abnormal<ref name="Clinical chemistry">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBGK/plasma-chemistry/ |title=Clinical chemistry data for Prkcz |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| [[Blood plasma|Plasma]] [[immunoglobulin]]s || bgcolor="#488ED3"|Normal
|-
| [[Haematology]] || bgcolor="#488ED3"|Normal
|-
| [[Micronucleus test]] || bgcolor="#488ED3"|Normal
|-
| Heart weight || bgcolor="#488ED3"|Normal
|-
| Tail epidermis wholemount || bgcolor="#488ED3"|Normal
|-
| Skin Histopathology || bgcolor="#C40000"|Abnormal
|-
| Brain histopathology || bgcolor="#488ED3"|Normal
|-
| ''[[Salmonella]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Salmonella'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBGK/salmonella-challenge/ |title=''Salmonella'' infection data for Prkcz |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| ''[[Citrobacter]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Citrobacter'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBGK/citrobacter-challenge/ |title=''Citrobacter'' infection data for Prkcz |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite web |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1755-3768.2010.4142.x/abstract |title=The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice |author=Gerdin AK |year=2010 |location=''Acta Opthalmologica'' '''88''': 925-7.doi:10.1111/j.1755-3768.2010.4142.x |publisher=Wiley}}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
|}
[[Model organism]]s have been used in the study of PRKCZ function. A conditional [[knockout mouse]] line, called ''Prkcz<sup>tm1a(EUCOMM)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Prkcz |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4433718 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{Cite pmid|21677750}}</ref><ref name="mouse_library">{{cite web |url=http://www.nature.com/news/2011/110615/full/474262a.html |title=Mouse library set to be knockout |author=Dolgin E |year=June 2011 |location=''Nature'' '''474''': 262-263. doi:10.1038/474262a}}</ref><ref name="mouse_for_all_reasons">{{cite book |title=A mouse for all reasons |author=Collins FS, Rossant J, Wurst W |year=January 2007 |location=''Cell'' '''128'''(1): 9-13. doi:10.1016/j.cell.2006.12.018 PMID 17218247}}</ref>

Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal| author=van der Weyden L, White JK, Adams DJ, Logan DW| title=The mouse genetics toolkit: revealing function and mechanism | journal=Genome Biol | year= 2011 | volume= 12 | issue= 6 | pages= 224 | pmid=21722353 | doi=10.1186/gb-2011-12-6-224 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21722353| pmc=3218837 }} </ref> Twenty five tests were carried out on [[mutant]] mice and three significant abnormalities were observed.<ref name="mgp_reference" /> Homozygous mutant males had [[Bergmeister's papilla]], while both sexes had atypical plasma chemistry and abnormal [[melanocyte]] morphology.<ref name="mgp_reference" />


==Interactions==
==Interactions==
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[[Category:Genes mutated in mice]]


{{Serine/threonine-specific protein kinases|g1}}
{{Serine/threonine-specific protein kinases|g1}}

Revision as of 00:07, 17 February 2012

Template:PBB Protein kinase C, zeta (PKCζ) also known as PRKCZ is an enzyme that in humans is encoded by the PRKCZ gene. The PRKCZ gene encodes at least two alternative transcripts, the full-length PKCζ and an N-terminal truncated form PKMζ. The truncated PKMζ is thought to be responsible for maintaining long-term memories in the brain.

Structure

PKC-zeta has an N-terminal regulatory domain, followed by a hinge region and a C-terminal catalytic domain. Second messengers stimulate PKCs by binding to the regulatory domain, translocating the enzyme from cytosol to membrane, and producing a conformational change that removes autoinhibition of the PKC catalytic activity. PKM-zeta, a brain-specific isoform of PKC-zeta generated from an alternative transcript, lacks the regulatory region of full-length PKC-zeta and is therefore constitutively active.[1]

PKMζ is the independent catalytic domain of protein kinase Cζ (PKCζ) and, lacking an autoinhibitory regulatory domain of the full-length PKCζ, is constitutively and persistently active, without the need of a second messenger. It was originally thought of as being a cleavage product of full-length PKCζ, an atypical isoform of protein kinase C (PKC). Like other PKC isoforms, PKCζ is a serine/threonine kinase that adds phosphate groups to target proteins. It is atypical in that unlike other PKC isoforms, PKCζ does not require calcium or diacylglycerol (DAG) to become active, but rather relies on a different second messenger, presumably generated through a phosphoinositide 3-kinase (PI3-kinase) pathway. It is now known that PKMζ is not the result of cleavage of full-length PKCζ, but rather, in the mammalian brain, is translated from its own brain-specific mRNA, that is transcribed by an internal promoter within the PKCζ gene.[1] The promoter for full-length PKCζ is largely inactive in the forebrain and so PKMζ is the dominant form of ζ in the forebrain and the only PKM that is translated from its own mRNA.

Function

PKCζ

Atypical PKC (aPKC) isoforms [zeta (this enzyme) and lambda/iota] play important roles in insulin-stimulated glucose transport. Human adipocytes contain PKC-zeta, rather than PKC-lambda/iota, as their major aPKC. Inhibition of the PKCζ enzyme inhibits insulin-stimulated glucose transport while activation of PKCζ increases glucose transport.[2]

PKMζ

PKMζ is thought to be responsible for maintaining the late phase of long-term potentiation (LTP).[3][4][5] This theory arose from the observation that PKMζ perfused post synaptically into neurons causes synaptic potentiation, and selective inhibitors of PKMζ, when bath applied one hour after tetanization, inhibit the late phase or maintenance of LTP. Thus PKMζ is both necessary and sufficient for maintaining LTP. Subsequent work showed that inhibiting PKMζ reversed LTP maintenance when applied up to 5 hours after LTP was induced in hippocampal slices, and after 22 hours in vivo. Inhibiting PKMζ in behaving animals erased spatial long-term memories in the hippocampus that were up to one month old, without affecting spatial short-term memories[5], and erased long-term memories for fear conditioning and inhibitory avoidance in the basolateral amygdala.[6] In the neocortex, thought to be the site of storage for most long-term memories, PKMζ inhibition erased associative memories for conditioned taste aversion in the insular cortex, up to 3 months after training.[7][8] PKMζ is thus the first molecule shown to be a component of the storage mechanism of long-term memory.

Recent research has demonstrated alteration in PKMζ in Alzheimer's disease (see Long-term potentiation), providing a potential link between this kinase and neurodegeneration.[9]

Model organisms

Model organisms have been used in the study of PRKCZ function. A conditional knockout mouse line, called Prkcztm1a(EUCOMM)Wtsi[16][17] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[18][19][20]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[14][21] Twenty five tests were carried out on mutant mice and three significant abnormalities were observed.[14] Homozygous mutant males had Bergmeister's papilla, while both sexes had atypical plasma chemistry and abnormal melanocyte morphology.[14]

Interactions

PRKCZ has been shown to interact with CENTA1,[22] PDPK1,[23][24][25][26] PARD6A,[27][28][29] Src,[30] NFATC2,[31] PAWR,[32] YWHAQ,[33] WWC1,[34] C-Raf,[33] AKT3,[35] PARD6B,[29] RELA,[36] FEZ1,[37] YWHAB,[33] FEZ2,[38] C1QBP,[39] YWHAZ[22][33] and MAP2K5.[40]

References

  1. ^ a b Hernandez AI, Blace N, Crary JF, Serrano PA, Leitges M, Libien JM, Weinstein G, Tcherapanov A, Sacktor TC (2003). "Protein kinase M zeta synthesis from a brain mRNA encoding an independent protein kinase C zeta catalytic domain. Implications for the molecular mechanism of memory". J. Biol. Chem. 278 (41): 40305–16. doi:10.1074/jbc.M307065200. PMID 12857744. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  2. ^ Bandyopadhyay G, Sajan MP, Kanoh Y, Standaert ML, Quon MJ, Lea-Currie R, Sen A, Farese RV (2002). "PKC-zeta mediates insulin effects on glucose transport in cultured preadipocyte-derived human adipocytes". J. Clin. Endocrinol. Metab. 87 (2): 716–23. doi:10.1210/jc.87.2.716. PMID 11836310. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ Ling D, Benardo L, Serrano P, Blace N, Kelly M, Crary J, Sacktor T (2002). "Protein kinase Mzeta is necessary and sufficient for LTP maintenance". Nat. Neurosci. 5 (4): 295–6. doi:10.1038/nn829. PMID 11914719.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Serrano P, Yao Y, Sacktor T (2005). "Persistent phosphorylation by protein kinase Mzeta maintains late-phase long-term potentiation". J Neurosci. 25 (8): 1979–84. doi:10.1523/JNEUROSCI.5132-04.2005. PMID 15728837.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ a b Pastalkova E, Serrano P, Pinkhasova D, Wallace E, Fenton A, Sacktor T (2006). "Storage of spatial information by the maintenance mechanism of LTP". Science. 313 (5790): 1141–4. doi:10.1126/science.1128657. PMID 16931766.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Serrano P; et al. (2008). "PKMζ maintains spatial, instrumental, and classically conditioned long-term memories". PLoS Biology. 6 (12): 2698–706. doi:10.1371/journal.pbio.0060318. PMC 2605920. PMID 19108606. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: unflagged free DOI (link)
  7. ^ Shema R, Sacktor T, Dudai Y (2007). "Rapid erasure of long-term memory associations in the cortex by an inhibitor of PKMζ". Science. 317 (5840): 951–3. doi:10.1126/science.1144334. PMID 17702943.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  9. ^ Crary JF, Shao CY, Mirra SS, Hernandez AI, Sacktor TC (2006). "Atypical protein kinase C in neurodegenerative disease I: PKMzeta aggregates with limbic neurofibrillary tangles and AMPA receptors in Alzheimer disease". J. Neuropathol. Exp. Neurol. 65 (4): 319–26. doi:10.1097/01.jnen.0000218442.07664.04. PMID 16691113. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ "Eye morphology data for Prkcz". Wellcome Trust Sanger Institute.
  11. ^ "Clinical chemistry data for Prkcz". Wellcome Trust Sanger Institute.
  12. ^ "Salmonella infection data for Prkcz". Wellcome Trust Sanger Institute.
  13. ^ "Citrobacter infection data for Prkcz". Wellcome Trust Sanger Institute.
  14. ^ a b c d Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Opthalmologica 88: 925-7.doi:10.1111/j.1755-3768.2010.4142.x: Wiley.{{cite web}}: CS1 maint: location (link)
  15. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  16. ^ "International Knockout Mouse Consortium".
  17. ^ "Mouse Genome Informatics".
  18. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 21677750, please use {{cite journal}} with |pmid=21677750 instead.
  19. ^ Dolgin E (June 2011). "Mouse library set to be knockout". Nature 474: 262-263. doi:10.1038/474262a.{{cite web}}: CS1 maint: location (link)
  20. ^ Collins FS, Rossant J, Wurst W (January 2007). A mouse for all reasons. Cell 128(1): 9-13. doi:10.1016/j.cell.2006.12.018 PMID 17218247.{{cite book}}: CS1 maint: location (link) CS1 maint: location missing publisher (link) CS1 maint: multiple names: authors list (link)
  21. ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  22. ^ a b Zemlickova, Eva (2003). "Centaurin-alpha(1) associates with and is phosphorylated by isoforms of protein kinase C". Biochem. Biophys. Res. Commun. 307 (3). United States: 459–65. doi:10.1016/S0006-291X(03)01187-2. ISSN 0006-291X. PMID 12893243. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
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  24. ^ Hodgkinson, Conrad P (2002). "Regulation of both PDK1 and the phosphorylation of PKC-zeta and -delta by a C-terminal PRK2 fragment". Biochemistry. 41 (2). United States: 561–9. doi:10.1021/bi010719z. ISSN 0006-2960. PMID 11781095. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  25. ^ Le Good, J A (1998). "Protein kinase C isotypes controlled by phosphoinositide 3-kinase through the protein kinase PDK1". Science. 281 (5385). UNITED STATES: 2042–5. doi:10.1126/science.281.5385.2042. ISSN 0036-8075. PMID 9748166. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  26. ^ Park, J (1999). "Serum and glucocorticoid-inducible kinase (SGK) is a target of the PI 3-kinase-stimulated signaling pathway". EMBO J. 18 (11). ENGLAND: 3024–33. doi:10.1093/emboj/18.11.3024. ISSN 0261-4189. PMC 1171384. PMID 10357815. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  27. ^ Rual, Jean-François (2005). "Towards a proteome-scale map of the human protein-protein interaction network". Nature. 437 (7062). England: 1173–8. doi:10.1038/nature04209. PMID 16189514. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  28. ^ Liu, Xiu-Fen (2004). "Nucleotide exchange factor ECT2 interacts with the polarity protein complex Par6/Par3/protein kinase Czeta (PKCzeta) and regulates PKCzeta activity". Mol. Cell. Biol. 24 (15). United States: 6665–75. doi:10.1128/MCB.24.15.6665-6675.2004. ISSN 0270-7306. PMC 444862. PMID 15254234. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  29. ^ a b Noda, Y (2001). "Human homologues of the Caenorhabditis elegans cell polarity protein PAR6 as an adaptor that links the small GTPases Rac and Cdc42 to atypical protein kinase C". Genes Cells. 6 (2). England: 107–19. doi:10.1046/j.1365-2443.2001.00404.x. ISSN 1356-9597. PMID 11260256. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  30. ^ Seibenhener, M L (1999). "Identification of Src as a novel atypical protein kinase C-interacting protein". Mol. Cell Biol. Res. Commun. 2 (1). UNITED STATES: 28–31. doi:10.1006/mcbr.1999.0140. ISSN 1522-4724. PMID 10527887. {{cite journal}}: Check date values in: |year= (help); Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  31. ^ San-Antonio, Belén (2002). "Protein kinase Czeta phosphorylates nuclear factor of activated T cells and regulates its transactivating activity". J. Biol. Chem. 277 (30). United States: 27073–80. doi:10.1074/jbc.M106983200. ISSN 0021-9258. PMID 12021260. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: unflagged free DOI (link)
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  40. ^ Diaz-Meco, M T (2001). "MEK5, a new target of the atypical protein kinase C isoforms in mitogenic signaling". Mol. Cell. Biol. 21 (4). United States: 1218–27. doi:10.1128/MCB.21.4.1218-1227.2001. ISSN 0270-7306. PMC 99575. PMID 11158308. {{cite journal}}: Check date values in: |year= (help); Cite has empty unknown parameters: |laydate=, |laysummary=, and |laysource= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

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