Concanavalin A affects β-tubulin mRNA expression during neuritic processes of mouse neuroblastoma N18TG2 cells in a different manner from colchicine

1990 ◽  
Vol 167 (3) ◽  
pp. 1348-1354 ◽  
Author(s):  
Noriko Katayama ◽  
Yukari Yamagata ◽  
Hirotaka Hashimoto ◽  
Hiroshi Kanazawa ◽  
Tomofusa Tsuchiya ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Concanavalin A ◽  
Mouse Neuroblastoma ◽  
Tubulin Mrna ◽  
Β Tubulin

scholarly journals Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries

2020 ◽  
Vol 68 (7) ◽  
pp. 1276-1281
Author(s):  
Jian Wang ◽  
Song-Yuan He
Keyword(s):  
Angiotensin Ii ◽  
Mrna Expression ◽  
Cell Apoptosis ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Apoptotic Cells ◽  
Qrt Pcr ◽  
Tubulin Mrna ◽  
Β Tubulin

This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and β-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and β-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and β-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.

scholarly journals Deadenylation-Dependent and -Independent Decay Pathways for α1-Tubulin mRNA in Chlamydomonas reinhardtii

1998 ◽  
Vol 18 (3) ◽  
pp. 1498-1505 ◽  
Author(s):  
Joseph F. Gera ◽  
Ellen J. Baker
Keyword(s):  
Chlamydomonas Reinhardtii ◽  
Northern Blot ◽  
Untranslated Region ◽  
Northern Blot Analysis ◽  
Actinomycin D ◽  
Degradation Pathway ◽  
Transformed Cells ◽  
Tubulin Mrna ◽  
Single Transcript ◽  
Β Tubulin

ABSTRACT The α- and β-tubulin mRNAs of Chlamydomonas reinhardtii exhibit different half-lives under different conditions: when expressed constitutively, they degrade with half-lives of about 1 h, whereas when induced by deflagellation, they degrade with half-lives of only 10 to 15 min. To investigate the decay pathway(s) used under these two conditions, an α1-tubulin gene construct which included an insert of 30 guanidylate residues within the 3′ untranslated region was introduced into cells. This transgene was efficiently expressed in stably transformed cells, and the mRNA exhibited constitutive and postinduction half-lives like those of the α1-tubulin mRNA. Northern blot analysis revealed the occurrence of a 3′ RNA fragment derived from the poly(G)-containing α1-tubulin transcripts. The 3′ fragment was shown to accumulate as full-length mRNA disappeared in actinomycin D-treated cells, indicating a precursor-product relationship. Insertion of a second poly(G) tract upstream of the first resulted in accumulation of only a longer 3′ fragment, suggesting that the decay intermediate is generated by 5′-to-3′ exonucleolytic digestion. A translational requirement for generation of the 3′ fragment was demonstrated by experiments in which cells were deflagellated in the presence of cycloheximide. Analysis of fragment poly(A) length revealed that the fragments were, at most, oligoadenylated in nondeflagellated cells but had a long poly(A) tail in deflagellated cells. These findings suggest that the oligoadenylated fragment is a decay intermediate in a deadenylation-dependent, constitutive degradation pathway and that the requirement for deadenylation is bypassed in deflagellated cells. This represents the first example in which a single transcript has been shown to be targeted to different decay pathways under different cellular conditions.

scholarly journals Photoregulation of β-Tubulin mRNA Abundance in Etiolated Oat and Barley Seedlings

1990 ◽  
Vol 93 (3) ◽  
pp. 1196-1202 ◽  
Author(s):  
James T. Colbert ◽  
Stephen A. Costigan ◽  
Zhifan Zhao
Keyword(s):  
Mrna Abundance ◽  
Tubulin Mrna ◽  
Β Tubulin

scholarly journals Exonic Sequences in the 5′ Untranslated Region of α-Tubulin mRNA Modulate trans Splicing inTrypanosoma brucei

1998 ◽  
Vol 18 (8) ◽  
pp. 4620-4628 ◽  
Author(s):  
Carlos López-Estraño ◽  
Christian Tschudi ◽  
Elisabetta Ullu
Keyword(s):  
Splice Site ◽  
Competition Assay ◽  
Splice Site Selection ◽  
Tubulin Gene ◽  
Branch Site ◽  
Trans Splicing ◽  
Tubulin Mrna ◽  
Splicing Efficiency ◽  
Β Tubulin

ABSTRACT Previous studies have identified a conserved AG dinucleotide at the 3′ splice site (3′SS) and a polypyrimidine (pPy) tract that are required for trans splicing of polycistronic pre-mRNAs in trypanosomatids. Furthermore, the pPy tract of the Trypanosoma brucei α-tubulin 3′SS region is required to specify accurate 3′-end formation of the upstream β-tubulin gene and transsplicing of the downstream α-tubulin gene. Here, we employed an in vivo cis competition assay to determine whether sequences other than those of the AG dinucleotide and the pPy tract were required for 3′SS identification. Our results indicate that a minimal α-tubulin 3′SS, from the putative branch site region to the AG dinucleotide, is not sufficient for recognition by thetrans-splicing machinery and that polyadenylation is strictly dependent on downstream trans splicing. We show that efficient use of the α-tubulin 3′SS is dependent upon the presence of exon sequences. Furthermore, β-tubulin, but not actin exon sequences or unrelated plasmid sequences, can replace α-tubulin exon sequences for accurate trans-splice-site selection. Taken together, these results support a model in which the informational content required for efficient trans splicing of the α-tubulin pre-mRNA includes exon sequences which are involved in modulation of trans-splicing efficiency. Sequences that positively regulate trans splicing might be similar tocis-splicing enhancers described in other systems.

scholarly journals Huganbuzure Granule Attenuates Concanavalin-A-Induced Immune Liver Injury in Mice via Regulating the Balance of Th1/Th2/Th17/Treg Cells and Inhibiting Apoptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Mengheng Wang ◽  
Hailong Yin ◽  
Yu Xia ◽  
Yijun Tu ◽  
Xinshuang Zou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Protein Expression ◽  
Mrna Expression ◽  
Concanavalin A ◽  
Underlying Mechanism ◽  
Treg Cells ◽  
Mouse Serum ◽  
Mrna Levels ◽  
Immune Balance ◽  
Jnk Activation

In Uygur medicine, Huganbuzure granule (HBG) is one of the classical prescriptions for liver protection. However, its role in immune liver injury remains unknown. This study evaluates the effect of HBG on concanavalin-A- (ConA-) induced immune liver injury and investigates its protective underlying mechanism. BALB/c mice were randomly divided into five groups (n = 24 mice per group): control, ConA, 1.6 g/kg HBG + ConA, 3.2 g/kg HBG + ConA, and 6 mg/kg prednisolone + ConA. HBG was intragastrically administrated once daily for ten consecutive days, prior to ConA (20 mg/kg) injection. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), superoxide dismutase (SOD), and malondialdehyde (MDA) in mouse serum were measured after ConA injection. Moreover, liver-related mRNA levels were evaluated by qPCR. The detection of liver-related proteins was assessed by immunohistochemistry and western blot analysis. Compared with the ConA group, HBG reduced the mRNA expression of IL-17A and IFN-γ and the protein expression of T-bet and ROR-γt. In addition, HBG increased the mRNA expression of IL-4 and TGF-β and protein expression of GATA3 and Foxp3, indicating that HBG regulated the balance of Th1/Th2 and Th17/Treg. Furthermore, HBG alleviated immune liver injury by reducing oxidative stress, inhibiting apoptosis, and decreasing the expression of p-JNK, p-ERK, p-p38, p-JAK1, p-STAT1, p-STAT3, and IRF1. Our data suggested that HBG attenuated ConA-induced immune liver injury by regulating the immune balance and inhibiting JAK1/STATs/IRF1 signaling, thereby reducing apoptosis induced by JNK activation. The findings indicate that HBG may be a promising drug for immune liver injury.

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