Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells
The klotho gene was identified in 1997 as the gene whose severe insufficiency (kl/kl) causes a syndrome resembling human aging, such as osteoporosis, arteriosclerosis, gonadal atrophy, emphysema, and short life span in a mouse strain. Regarding the gait disturbance reported in kl/kl mice, the presen...
Gespeichert in:
| Veröffentlicht in: | Acta neuropathologica 2005-05, Vol.109 (5), p.457-466 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 466 |
|---|---|
| container_issue | 5 |
| container_start_page | 457 |
| container_title | Acta neuropathologica |
| container_volume | 109 |
| creator | Anamizu, Yorito Kawaguchi, Hiroshi Seichi, Atsushi Yamaguchi, Shinji Kawakami, Emiko Kanda, Naotoshi Matsubara, Shiro Kuro-o, Makoto Nabeshima, Yoichi Nakamura, Kozo Oyanagi, Kiyomitsu |
| description | The klotho gene was identified in 1997 as the gene whose severe insufficiency (kl/kl) causes a syndrome resembling human aging, such as osteoporosis, arteriosclerosis, gonadal atrophy, emphysema, and short life span in a mouse strain. Regarding the gait disturbance reported in kl/kl mice, the present study examined the spinal cord of kl/kl mice, and revealed decreases in the number of large anterior horn cells (AHCs), the amount of cytoplasmic RNA, the number of ribosomes and rough endoplasmic reticulum (rER), and the activity of ribosomal (r) RNA gene transcription without significant loss of the total number of neurons in the ventral gray matter. Increased immunostaining of phosphorylated neurofilament in the AHCs and of glial fibrillary acidic protein in reactive astrocytes in the anterior horn of kl/kl mice were also observed. On the other hand, the posterior horn was quite well preserved. The results suggest that the kl/kl insufficiency causes atrophy and dysfunction of the spinal AHCs through decreased activity of rRNA gene transcription, which may reduce the amount of cytoplasmic RNA and the number of ribosomes and rER. These findings resemble those found in the spinal cord of patients with classic amyotrophic lateral sclerosis (ALS). The results show that klotho gene insufficiency causes dysfunction of the protein synthesizing system in the AHCs, and might indicate the klotho gene is involved in the pathological mechanism of classic ALS. The kl/kl is a new animal model of AHC degeneration, and may provide clues to understanding the etiology of classic ALS. |
| doi_str_mv | 10.1007/s00401-004-0971-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67930354</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67930354</sourcerecordid><originalsourceid>FETCH-LOGICAL-c392t-dd75388842388c76c82aff0642a0e253d9358471a45b6d2659ee0ffcb75ec4b53</originalsourceid><addsrcrecordid>eNpdkc2KFTEQhYMoznX0AdxIcOHK1vx2upfDMP7goDDoOqTT1XMzdCdtKi3cx_CNzfVeENycoqivThUcQl5y9o4zZt4jY4rxpmrDesMb84jsuJKiYVrKx2THWJ22UogL8gzxoXbCKP2UXHDdSWWk2JHfX-ZU9omGiNs0BR8g-gP1bkNAOoLP4BBommgOQ8K0uJnefb2i9xCBluwi-hzWElKkzpfwK5TDW-oPJa2zwyX4v7CLI81pu9_Tm7t6iJY9UFxDrF4uFsghZbpPOVIP84zPyZPJzQgvzvWS_Phw8_36U3P77ePn66vbxstelGYcjZZd1ylR1ZvWd8JNE2uVcAyElmMvdacMd0oP7Sha3QOwafKD0eDVoOUleXPyXXP6uQEWuwQ8fuAipA1ta3rJpFYVfP0f-JC2XL9HKzg3PdesrxA_QT4nxAyTXXNYXD5YzuwxLHsKy1a1x7CsqTuvzsbbsMD4b-OcjvwDEMqQvA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>211791509</pqid></control><display><type>article</type><title>Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Anamizu, Yorito ; Kawaguchi, Hiroshi ; Seichi, Atsushi ; Yamaguchi, Shinji ; Kawakami, Emiko ; Kanda, Naotoshi ; Matsubara, Shiro ; Kuro-o, Makoto ; Nabeshima, Yoichi ; Nakamura, Kozo ; Oyanagi, Kiyomitsu</creator><creatorcontrib>Anamizu, Yorito ; Kawaguchi, Hiroshi ; Seichi, Atsushi ; Yamaguchi, Shinji ; Kawakami, Emiko ; Kanda, Naotoshi ; Matsubara, Shiro ; Kuro-o, Makoto ; Nabeshima, Yoichi ; Nakamura, Kozo ; Oyanagi, Kiyomitsu</creatorcontrib><description>The klotho gene was identified in 1997 as the gene whose severe insufficiency (kl/kl) causes a syndrome resembling human aging, such as osteoporosis, arteriosclerosis, gonadal atrophy, emphysema, and short life span in a mouse strain. Regarding the gait disturbance reported in kl/kl mice, the present study examined the spinal cord of kl/kl mice, and revealed decreases in the number of large anterior horn cells (AHCs), the amount of cytoplasmic RNA, the number of ribosomes and rough endoplasmic reticulum (rER), and the activity of ribosomal (r) RNA gene transcription without significant loss of the total number of neurons in the ventral gray matter. Increased immunostaining of phosphorylated neurofilament in the AHCs and of glial fibrillary acidic protein in reactive astrocytes in the anterior horn of kl/kl mice were also observed. On the other hand, the posterior horn was quite well preserved. The results suggest that the kl/kl insufficiency causes atrophy and dysfunction of the spinal AHCs through decreased activity of rRNA gene transcription, which may reduce the amount of cytoplasmic RNA and the number of ribosomes and rER. These findings resemble those found in the spinal cord of patients with classic amyotrophic lateral sclerosis (ALS). The results show that klotho gene insufficiency causes dysfunction of the protein synthesizing system in the AHCs, and might indicate the klotho gene is involved in the pathological mechanism of classic ALS. The kl/kl is a new animal model of AHC degeneration, and may provide clues to understanding the etiology of classic ALS.</description><identifier>ISSN: 0001-6322</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s00401-004-0971-7</identifier><identifier>PMID: 15834732</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Animals ; Body Weight - genetics ; Brain - pathology ; Cell Count - methods ; Cell Nucleolus - genetics ; Cytoplasm - genetics ; Cytoplasm - metabolism ; Endoplasmic Reticulum - genetics ; Endoplasmic Reticulum - metabolism ; Glial Fibrillary Acidic Protein - metabolism ; Glucuronidase ; Immunohistochemistry - methods ; Male ; Membrane Proteins - deficiency ; Mice ; Mice, Knockout ; Microscopy, Electron, Transmission ; Neurofilament Proteins - metabolism ; Organ Size - genetics ; Posterior Horn Cells - metabolism ; Posterior Horn Cells - physiology ; Posterior Horn Cells - ultrastructure ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA - metabolism ; RNA, Messenger - biosynthesis ; RNA, Ribosomal - genetics ; RNA, Ribosomal - metabolism ; Spinal Cord - metabolism ; Spinal Cord - ultrastructure ; Transcription, Genetic - physiology</subject><ispartof>Acta neuropathologica, 2005-05, Vol.109 (5), p.457-466</ispartof><rights>Springer-Verlag 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-dd75388842388c76c82aff0642a0e253d9358471a45b6d2659ee0ffcb75ec4b53</citedby><cites>FETCH-LOGICAL-c392t-dd75388842388c76c82aff0642a0e253d9358471a45b6d2659ee0ffcb75ec4b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15834732$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Anamizu, Yorito</creatorcontrib><creatorcontrib>Kawaguchi, Hiroshi</creatorcontrib><creatorcontrib>Seichi, Atsushi</creatorcontrib><creatorcontrib>Yamaguchi, Shinji</creatorcontrib><creatorcontrib>Kawakami, Emiko</creatorcontrib><creatorcontrib>Kanda, Naotoshi</creatorcontrib><creatorcontrib>Matsubara, Shiro</creatorcontrib><creatorcontrib>Kuro-o, Makoto</creatorcontrib><creatorcontrib>Nabeshima, Yoichi</creatorcontrib><creatorcontrib>Nakamura, Kozo</creatorcontrib><creatorcontrib>Oyanagi, Kiyomitsu</creatorcontrib><title>Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><description>The klotho gene was identified in 1997 as the gene whose severe insufficiency (kl/kl) causes a syndrome resembling human aging, such as osteoporosis, arteriosclerosis, gonadal atrophy, emphysema, and short life span in a mouse strain. Regarding the gait disturbance reported in kl/kl mice, the present study examined the spinal cord of kl/kl mice, and revealed decreases in the number of large anterior horn cells (AHCs), the amount of cytoplasmic RNA, the number of ribosomes and rough endoplasmic reticulum (rER), and the activity of ribosomal (r) RNA gene transcription without significant loss of the total number of neurons in the ventral gray matter. Increased immunostaining of phosphorylated neurofilament in the AHCs and of glial fibrillary acidic protein in reactive astrocytes in the anterior horn of kl/kl mice were also observed. On the other hand, the posterior horn was quite well preserved. The results suggest that the kl/kl insufficiency causes atrophy and dysfunction of the spinal AHCs through decreased activity of rRNA gene transcription, which may reduce the amount of cytoplasmic RNA and the number of ribosomes and rER. These findings resemble those found in the spinal cord of patients with classic amyotrophic lateral sclerosis (ALS). The results show that klotho gene insufficiency causes dysfunction of the protein synthesizing system in the AHCs, and might indicate the klotho gene is involved in the pathological mechanism of classic ALS. The kl/kl is a new animal model of AHC degeneration, and may provide clues to understanding the etiology of classic ALS.</description><subject>Animals</subject><subject>Body Weight - genetics</subject><subject>Brain - pathology</subject><subject>Cell Count - methods</subject><subject>Cell Nucleolus - genetics</subject><subject>Cytoplasm - genetics</subject><subject>Cytoplasm - metabolism</subject><subject>Endoplasmic Reticulum - genetics</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Glucuronidase</subject><subject>Immunohistochemistry - methods</subject><subject>Male</subject><subject>Membrane Proteins - deficiency</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Electron, Transmission</subject><subject>Neurofilament Proteins - metabolism</subject><subject>Organ Size - genetics</subject><subject>Posterior Horn Cells - metabolism</subject><subject>Posterior Horn Cells - physiology</subject><subject>Posterior Horn Cells - ultrastructure</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA - metabolism</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Ribosomal - genetics</subject><subject>RNA, Ribosomal - metabolism</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - ultrastructure</subject><subject>Transcription, Genetic - physiology</subject><issn>0001-6322</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkc2KFTEQhYMoznX0AdxIcOHK1vx2upfDMP7goDDoOqTT1XMzdCdtKi3cx_CNzfVeENycoqivThUcQl5y9o4zZt4jY4rxpmrDesMb84jsuJKiYVrKx2THWJ22UogL8gzxoXbCKP2UXHDdSWWk2JHfX-ZU9omGiNs0BR8g-gP1bkNAOoLP4BBommgOQ8K0uJnefb2i9xCBluwi-hzWElKkzpfwK5TDW-oPJa2zwyX4v7CLI81pu9_Tm7t6iJY9UFxDrF4uFsghZbpPOVIP84zPyZPJzQgvzvWS_Phw8_36U3P77ePn66vbxstelGYcjZZd1ylR1ZvWd8JNE2uVcAyElmMvdacMd0oP7Sha3QOwafKD0eDVoOUleXPyXXP6uQEWuwQ8fuAipA1ta3rJpFYVfP0f-JC2XL9HKzg3PdesrxA_QT4nxAyTXXNYXD5YzuwxLHsKy1a1x7CsqTuvzsbbsMD4b-OcjvwDEMqQvA</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>Anamizu, Yorito</creator><creator>Kawaguchi, Hiroshi</creator><creator>Seichi, Atsushi</creator><creator>Yamaguchi, Shinji</creator><creator>Kawakami, Emiko</creator><creator>Kanda, Naotoshi</creator><creator>Matsubara, Shiro</creator><creator>Kuro-o, Makoto</creator><creator>Nabeshima, Yoichi</creator><creator>Nakamura, Kozo</creator><creator>Oyanagi, Kiyomitsu</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20050501</creationdate><title>Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells</title><author>Anamizu, Yorito ; Kawaguchi, Hiroshi ; Seichi, Atsushi ; Yamaguchi, Shinji ; Kawakami, Emiko ; Kanda, Naotoshi ; Matsubara, Shiro ; Kuro-o, Makoto ; Nabeshima, Yoichi ; Nakamura, Kozo ; Oyanagi, Kiyomitsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-dd75388842388c76c82aff0642a0e253d9358471a45b6d2659ee0ffcb75ec4b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Body Weight - genetics</topic><topic>Brain - pathology</topic><topic>Cell Count - methods</topic><topic>Cell Nucleolus - genetics</topic><topic>Cytoplasm - genetics</topic><topic>Cytoplasm - metabolism</topic><topic>Endoplasmic Reticulum - genetics</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Glucuronidase</topic><topic>Immunohistochemistry - methods</topic><topic>Male</topic><topic>Membrane Proteins - deficiency</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Electron, Transmission</topic><topic>Neurofilament Proteins - metabolism</topic><topic>Organ Size - genetics</topic><topic>Posterior Horn Cells - metabolism</topic><topic>Posterior Horn Cells - physiology</topic><topic>Posterior Horn Cells - ultrastructure</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA - metabolism</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Ribosomal - genetics</topic><topic>RNA, Ribosomal - metabolism</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - ultrastructure</topic><topic>Transcription, Genetic - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Anamizu, Yorito</creatorcontrib><creatorcontrib>Kawaguchi, Hiroshi</creatorcontrib><creatorcontrib>Seichi, Atsushi</creatorcontrib><creatorcontrib>Yamaguchi, Shinji</creatorcontrib><creatorcontrib>Kawakami, Emiko</creatorcontrib><creatorcontrib>Kanda, Naotoshi</creatorcontrib><creatorcontrib>Matsubara, Shiro</creatorcontrib><creatorcontrib>Kuro-o, Makoto</creatorcontrib><creatorcontrib>Nabeshima, Yoichi</creatorcontrib><creatorcontrib>Nakamura, Kozo</creatorcontrib><creatorcontrib>Oyanagi, Kiyomitsu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Acta neuropathologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Anamizu, Yorito</au><au>Kawaguchi, Hiroshi</au><au>Seichi, Atsushi</au><au>Yamaguchi, Shinji</au><au>Kawakami, Emiko</au><au>Kanda, Naotoshi</au><au>Matsubara, Shiro</au><au>Kuro-o, Makoto</au><au>Nabeshima, Yoichi</au><au>Nakamura, Kozo</au><au>Oyanagi, Kiyomitsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells</atitle><jtitle>Acta neuropathologica</jtitle><addtitle>Acta Neuropathol</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>109</volume><issue>5</issue><spage>457</spage><epage>466</epage><pages>457-466</pages><issn>0001-6322</issn><eissn>1432-0533</eissn><abstract>The klotho gene was identified in 1997 as the gene whose severe insufficiency (kl/kl) causes a syndrome resembling human aging, such as osteoporosis, arteriosclerosis, gonadal atrophy, emphysema, and short life span in a mouse strain. Regarding the gait disturbance reported in kl/kl mice, the present study examined the spinal cord of kl/kl mice, and revealed decreases in the number of large anterior horn cells (AHCs), the amount of cytoplasmic RNA, the number of ribosomes and rough endoplasmic reticulum (rER), and the activity of ribosomal (r) RNA gene transcription without significant loss of the total number of neurons in the ventral gray matter. Increased immunostaining of phosphorylated neurofilament in the AHCs and of glial fibrillary acidic protein in reactive astrocytes in the anterior horn of kl/kl mice were also observed. On the other hand, the posterior horn was quite well preserved. The results suggest that the kl/kl insufficiency causes atrophy and dysfunction of the spinal AHCs through decreased activity of rRNA gene transcription, which may reduce the amount of cytoplasmic RNA and the number of ribosomes and rER. These findings resemble those found in the spinal cord of patients with classic amyotrophic lateral sclerosis (ALS). The results show that klotho gene insufficiency causes dysfunction of the protein synthesizing system in the AHCs, and might indicate the klotho gene is involved in the pathological mechanism of classic ALS. The kl/kl is a new animal model of AHC degeneration, and may provide clues to understanding the etiology of classic ALS.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>15834732</pmid><doi>10.1007/s00401-004-0971-7</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0001-6322 |
| ispartof | Acta neuropathologica, 2005-05, Vol.109 (5), p.457-466 |
| issn | 0001-6322 1432-0533 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67930354 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Body Weight - genetics Brain - pathology Cell Count - methods Cell Nucleolus - genetics Cytoplasm - genetics Cytoplasm - metabolism Endoplasmic Reticulum - genetics Endoplasmic Reticulum - metabolism Glial Fibrillary Acidic Protein - metabolism Glucuronidase Immunohistochemistry - methods Male Membrane Proteins - deficiency Mice Mice, Knockout Microscopy, Electron, Transmission Neurofilament Proteins - metabolism Organ Size - genetics Posterior Horn Cells - metabolism Posterior Horn Cells - physiology Posterior Horn Cells - ultrastructure Reverse Transcriptase Polymerase Chain Reaction - methods RNA - metabolism RNA, Messenger - biosynthesis RNA, Ribosomal - genetics RNA, Ribosomal - metabolism Spinal Cord - metabolism Spinal Cord - ultrastructure Transcription, Genetic - physiology |
| title | Klotho insufficiency causes decrease of ribosomal RNA gene transcription activity, cytoplasmic RNA and rough ER in the spinal anterior horn cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T23%3A49%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Klotho%20insufficiency%20causes%20decrease%20of%20ribosomal%20RNA%20gene%20transcription%20activity,%20cytoplasmic%20RNA%20and%20rough%20ER%20in%20the%20spinal%20anterior%20horn%20cells&rft.jtitle=Acta%20neuropathologica&rft.au=Anamizu,%20Yorito&rft.date=2005-05-01&rft.volume=109&rft.issue=5&rft.spage=457&rft.epage=466&rft.pages=457-466&rft.issn=0001-6322&rft.eissn=1432-0533&rft_id=info:doi/10.1007/s00401-004-0971-7&rft_dat=%3Cproquest_cross%3E67930354%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=211791509&rft_id=info:pmid/15834732&rfr_iscdi=true |