55,159 research outputs found
C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis
Full text linkUnderstanding the regulation of the apoptotic program in neurons by intracellular pathways is currently a subject of great interest. Recent results suggest that c-Jun N-terminal kinases (JNK), mitogen-activated protein kinases and the transcription factor c-Jun are important regulators of this cell death program in post-mitotic neurons following survival-factor withdrawal. Our study demonstrates that ceramide levels increase upon survival-factor withdrawal in primary cultured cortical neurons. Furthermore, survival-factor withdrawal or addition of exogenous c2-ceramide induces JNK pathway activation in these cells. Western blot analyses of JNK and c-Jun using phospho-specific antibodies reveal that JNK and subsequent c-Jun phosphorylation occur hours before the initiation of apoptosis, reflected morphologically by neurite retraction and fragmentation, cell-body shrinkage and chromatin fragmentation. Immunocytochemistry using the same antibodies shows that phospho-JNK are localized in the neurites of control neurons and translocate to the nucleus where phospho-c-Jun concurrently appears upon ceramide-induced apoptosis. To determine if ceramide-induced c-Jun activation is responsible for the induction of the apoptotic program, we performed transient transfections of a dominant negative form of c-Jun, truncated in its transactivation region. Our results show that DNc-Jun partially protects cortical neurons from ceramide-induced apoptosis. Treatment of dominant negative c-Jun-expressing neurons with the pharmacological inhibitor of p38 kinase, SB203580, completely blocked neuronal death. Thus our data show that p38 and JNK/c-Jun pathways cooperate to induce neuronal apoptosis
Devolia orientalis Li Bing Zhang, X. M. Zhou, Jian Jun Yang & Ralf Knapp 2023, comb. nov.
No full textDevolia orientalis (T.C.Hsu) Li Bing Zhang, X.M.Zhou, Jian Jun Yang & Ralf Knapp, comb. nov. Basionym: Oreogrammitis orientalis T.C.Hsu, Ferns Fern Allies Taiwan Second Suppl. 44. 2017. Type: China, Guangxi Zhuang Autonomous Region, Jinxiu Yao Autonomous County, Mt. Shengtang (ShengTangShan), 1800–1900 m, 2 April 2013, T.C.Hsu 6455 (holotype TAIF; isotypes AK, IBK, TAIF, TNM). This species occurs in Taiwan Island, Mainland China (Guangxi), and Japan (Knapp & Hsu, 2017).Published as part of Yang, Jian-Jun, Parris, Barbara, Knapp, Ralf, Sundue, Michael, Zhang, Li-Bing & Zhou, Xin-Mao, 2023, Circumscription of the grammitid fern genus Oreogrammitis (Polypodiaceae) with the description of three new genera: Calligrammitis, Devolia, and Glabrigrammitis, pp. 28-36 in Phytotaxa 597 (1) on page 34, DOI: 10.11646/phytotaxa.597.1.4, http://zenodo.org/record/791877
Glabrigrammitis nuda Li Bing Zhang, X. M. Zhou, Jian Jun Yang & Parris. 2023, comb. nov.
No full text<p> <i>Glabrigrammitis nuda</i> (Tagawa) Li Bing Zhang, X.M.Zhou, Jian Jun Yang & Parris, <i>comb. nov.</i></p> <p> Basionym: <i>Grammitis nuda</i> Tagawa,Acta Phytotax. Geobot. 10(4): 284. 1941.</p> <p> Type: Formosa (Taiwan), Takaio, between Daizyurin and Taito border, Tyosyo-gun, c. 1000 m, 22 January 1939, <i>Tagawa 2092</i> (holotype KYO!)</p> <p> ≡ <i>Oreogrammitis nuda</i> (Tagawa) Parris, Gard. Bull. Singapore 58(2): 264, 2007.</p> <p>This species is endemic to Taiwan Island.</p>Published as part of <i>Yang, Jian-Jun, Parris, Barbara, Knapp, Ralf, Sundue, Michael, Zhang, Li-Bing & Zhou, Xin-Mao, 2023, Circumscription of the grammitid fern genus Oreogrammitis (Polypodiaceae) with the description of three new genera: Calligrammitis, Devolia, and Glabrigrammitis, pp. 28-36 in Phytotaxa 597 (1)</i> on page 34, DOI: 10.11646/phytotaxa.597.1.4, <a href="http://zenodo.org/record/7918770">http://zenodo.org/record/7918770</a>
Glabrigrammitis subevenosa Li Bing Zhang, X. M. Zhou, Jian Jun Yang & Parris 2023, comb. nov.
No full textGlabrigrammitis subevenosa (Baker) Li Bing Zhang, X.M.Zhou, Jian Jun Yang & Parris, comb. nov. Basionym: Polypodium subevenosum Baker, Syn. Filic. (Hooker & Baker) 320. 1867. Type: [Malaysia] Penang, Mactier s.n. (holotype K001044343!; isotypes E00195211!, 00195212!) ≡ Grammitis subevenosa (Baker) C.Chr. & Tardieu, Notul. Syst. (Paris) 8: 179. 1939 ≡ Oreogrammitis subevenosa (Baker) Parris, Fern Gaz. 19(6): 207. 2013 = Grammitis sessilifolia J.Sm., Hist. Filic. 181. 1875, nom. nov. pro Polypodium sessilifolium Hook., Sp. Filic. 4: 168. 1863 non Liebm. 1849. Type [Malaysia] Malacca, Cuming 382 (lectotype K000784941!; designated here by Parris to replace Cuming 222 K000784942!, selected as lectotype by Parris, 1983; the latter is the specimen illustrated by Hooker, tab. CCLXXII A, but is not listed as a type) = P. malaicum Alderw., Malayan Ferns 577. 1909, nom. nov. pro P. sessilifolium Hook. 1863 non Liebm. 1849 ≡ G. malaica (Alderw.) Tagawa, Acta Phytotax. Geobot. 8: 173. 1939, nom. superfl. pro G. sessilifolia J.Sm. = P. maxwellii Baker, Bull. Misc. Inform., Kew 1893: 221. 1893. Type: Borneo, Sarawak, Mt Gading, 1891, Hose 296 (holotype K000547579!; isotypes E00194230!, SAR! both 1892, but labelled as type by Hose) ≡ G. maxwellii (Baker) Parris, Fern Gaz. 12(2): 118. 1980. This species occurs in Southeast Asia, Malesia, and Solomon Islands.Published as part of Yang, Jian-Jun, Parris, Barbara, Knapp, Ralf, Sundue, Michael, Zhang, Li-Bing & Zhou, Xin-Mao, 2023, Circumscription of the grammitid fern genus Oreogrammitis (Polypodiaceae) with the description of three new genera: Calligrammitis, Devolia, and Glabrigrammitis, pp. 28-36 in Phytotaxa 597 (1) on page 34, DOI: 10.11646/phytotaxa.597.1.4, http://zenodo.org/record/791877
Cissampelos keniensis Y. D. Zhou & Q. F. Wang
No full textE Cissampelos keniensis Y.D.Zhou & Q.F.Wang — Habit: Liana. Habitat: LMWF; 2 000–2 300 m. Distribution: IIIc. Voucher: Kaburia Track, Alt. 2 241 m, 29 Jun. 2016, Zhou & Mbuni 16/14 (HIB, EA, PE). Reference: Zhou et al. (2017b).Published as part of Zhou, Ya-Dong, Mwachala, Geoffrey, Hu, Guang-Wan & Wang, Qing-Feng, 2022, Annotated checklist of the vascular plants of Mount Kenya, East Africa, pp. 1-108 in Phytotaxa 546 (1) on page 41, DOI: 10.11646/phytotaxa.546.1.1, http://zenodo.org/record/655046
Megatachycines Zhu & Shi & Zhou 2022, gen. nov.
No full textGenus Megatachycines gen. nov. urn:lsid:zoobank.org:act: C46D40D4-C6B3-4B4A-988A-FD485EF01907 Type species Megatachycines pentus gen. et sp. nov., here designated. Diagnosis Body medium-sized for Aemodogryllini. Hind femur with inner spines on ventral surface. Male abdominal tergites without any processes. Male epiproct extended backward, distinctly longer than paraproct, quadrangular or pentagonal. Male paraproct slightly enlarged. Dorso-lateral lobes of male genitalia distinctly sclerotized. Male subgenital plate bilobed in the apical area. Female abdominal tergites without outgrowth. Remarks The new genus can easily be distinguished from other known genera of Aemodogryllini by the shapes of the male epiproct, dorso-lateral lobes of the male genitalia, and the male subgenital plate.Published as part of Zhu, Qi-Di, Shi, Fu-Ming & Zhou, Zhi-Jun, 2022, Notes on the genus Microtachycines Gorochov, 1992 and establishment of a new genus from China (Rhaphidophoridae: Aemodogryllinae), pp. 1-10 in European Journal of Taxonomy 817 on page 4, DOI: 10.5852/ejt.2022.817.1757, http://zenodo.org/record/651786
Proto-oncogene c-jun expression is induced by AML1-ETO in a JNK dependent manner:possible role in the pathogenesis of acute myeloid leukemia
Full text linkOverexpression of proto-oncogene c-jun and constitutive activation of the Jun NH2-terminal kinase (JNK) signaling pathway have been implicated in the leukemic transformation process. However, c-jun expression has not been investigated in acute myeloid leukemia (AML) cells containing the most common chromosomal translocations. t(8;21) is one of the most common AML-associated translocation and results in the AML1-ETO fusion protein. Overexpression of AML1-ETO in NIH3T3 cells leads to increased phosphorylation of Ser63 in c-Jun, which is generally JNK dependent. The role of the JNK signaling pathway for the functional properties of AML1-ETO is, however, unknown.
In the present study we found high expression levels of c-jun mRNA in t(8;21), t(15;17) or inv(16) positive patient cells by microarray analysis. Within t(8;21) positive patient samples, there was a correlation between AML1-ETO and c-jun mRNA expression levels. In myeloid U937 cells, c-jun mRNA and c-Jun protein expression levels increased upon induction of AML1-ETO. AML1-ETO transactivated the human c-jun promoter through the proximal AP-1 site via activating the JNK signaling pathway. JNK targets c-Jun and ATF-2, which also bind to the proximal AP-1 site in U937 cells, were also phosphorylated upon AML1-ETO induction. Furthermore, AML1-ETO induction increased the DNA binding capacity of c-Jun and ATF-2 to the proximal AP-1 site of the c-jun promoter, which might result in their enhanced transactivation capacities.
Interference with JNK and c-Jun activation by using JIP-1 or a JNK inhibitor reduced the transactivation capacity of AML1-ETO on the c-jun promoter and the pro-apoptotic function of AML1-ETO in U937 cells. AML1-ETO seems to activate the JNK signaling pathway by inducing the expression of a cytoplasmic factor, possibly G-CSF, because supernatant of AML1-ETO expressing cells was sufficient to induce phosphorylation of JNK and c-Jun in wildtype U937 cells.
This data demonstrates a novel mechanism of how AML1-ETO might exert positive effects on target gene expression and identifies the proto-oncogene c-jun as a common target gene in AML patient cells.Überexpression des Proto-Onkogens c-jun und konstitutive Aktivierung des Jun NH2-terminalen Kinase (JNK)-Signaltransduktionsweges sind wichtig für die leukämische Transformation in der Chronischen Myeloischen Leukämie. Die Expression von c-jun bei Akuter Myeloischer Leukämie (AML) mit den häufigsten reziproken Translokationen ist jedoch unbekannt. Bei einer der häufigsten AML Translokation t(8;21) wurde in Fibroblastenzellen gezeigt, daß das AML1-ETO-Fusionsgen die Phosphorylierung des Serin 63 in c-Jun erhöht. Die Rolle des JNK-Signalweges, der c-Jun am Serin 63 phosphorylieren kann, für die Funktion von AML1-ETO wurde bisher jedoch nicht untersucht. Weiterhin kann aktiviertes c-Jun durch eine positive Rückkoppelungsschleife über den c-jun Promotor zur Erhöhung der c-Jun Expression führen.
In der vorliegenden Arbeit konnten wir zeigen, daß AML Patientenzellen mit den häufigen Translokationen: t(8;21), t(15;17) oder inv(16) mehr c-jun mRNA besitzen im Vergleich zu Knochenmarkszellen gesunder Probanden. Weiterhin fanden wir eine hohe Korrelation zwischen der AML1-ETO und der c-jun mRNA bei t(8;21) positiven Patientenzellen. Induktion von AML1-ETO in der myeloischen U937 Zellinie erhöhte sowohl c-jun mRNA als auch c-Jun Proteinexpression. Damit konnten wir zeigen, daß AML1-ETO die Erhöhung der c-jun Expression bewirkt. Wir untersuchten den molekularen Mechanismus in U937 Zellen mittels transienter Transfektionen und fanden, daß AML1-ETO den c-jun Promotor durch die proximale AP-1 Seite transaktiviert. Diese Transaktivierung erfolgte indirekt über Aktivierung des JNK-Signaltransduktionsweges durch AML1-ETO. AML1-ETO-Induktion führte auch zur Phosphorylierung der JNK-Zielproteine c-Jun und ATF-2. Diese konnten im Gelretardierungsassay an die proximale AP-1 Seite des c-jun Promotors binden und wurden durch AML1-ETO-Induktion in ihrer Bindungsfähigkeit verstärkt. Deshalb nehmen wir an, daß die Transaktivierungskapazität des c-jun Promotors durch AML1-ETO über die Aktivierung des JNK-Signalweges läuft
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