Human Apoptosis Antagonizing Transcription Factor ELISA , AATF
- Known as:
- Human Apoptosis Antagonizing Transcription Factor Enzyme-linked immunosorbent assay test , AATF
- Catalog number:
- E01A0531
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Apoptosis Antagonizing Transcription Factor ELISA AATF
Ask about this productRelated genes to: Human Apoptosis Antagonizing Transcription Factor ELISA , AATF
- Gene:
- AATF NIH gene
- Name:
- apoptosis antagonizing transcription factor
- Previous symbol:
- -
- Synonyms:
- DED, CHE-1, CHE1, BFR2
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-13
- Date modifiied:
- 2015-01-29
Related products to: Human Apoptosis Antagonizing Transcription Factor ELISA , AATF
Related articles to: Human Apoptosis Antagonizing Transcription Factor ELISA , AATF
- Metabolic dysfunction-associated steatohepatitis-driven hepatocellular carcinoma (MASH-HCC) is a global clinical challenge for which there is a limited understanding of disease pathogenesis and a subsequent lack of therapeutic interventions. We previously identified that tumor necrosis factor-alpha (TNF-α) upregulated apoptosis antagonizing transcription factor (AATF) in MASH. Here, we investigated the effect of TNF-α converting enzyme (TACE) inhibition as a promising targeted therapy against AATF-mediated steatohepatitis to hepatocarcinogenesis. A preclinical murine model that recapitulates human MASH-HCC was used in the study. C57Bl/6 mice were fed with chow diet normal water (CD) or western diet sugar water (WD) along with a low dose of carbon tetrachloride (CCl; 0.2 μL·g, weekly) for 24 weeks. TACE activity, TNF-α levels, and AATF expression were measured. The mice were treated with the TACE inhibitor Marimastat for 12 weeks, followed by analyses of liver injury, fibrosis, inflammation, and oncogenic signaling. In vitro experiments using stable clones of AATF control and AATF knockdown were also conducted. We found that AATF expression was upregulated in WD/CCl mice, which developed severe MASH at 12 weeks and advanced fibrosis with HCC at 24 weeks. WD/CCl mice showed increased TACE activity with reduced hepatic expression of sirtuin 1 (Sirt1) and tissue inhibitor of metalloproteinase 3 (Timp3). The involvement of the SIRT1/TIMP3/TACE axis was confirmed by the release of TNF-α, which upregulated AATF, a key molecular driver of MASH-HCC. Interestingly, TACE inhibition by Marimastat reduced liver injury, dyslipidemia, AATF expression, and oncogenic signaling, effectively preventing hepatocarcinogenesis. Furthermore, Marimastat inhibited the activation of JNK, ERK1/2, and AKT, which are key regulators of tumorigenesis in WD/CCl mice and in AATF control cells, but had no effect on AATF knockdown cells. This study shows that TACE inhibition prevents AATF-mediated inflammation, fibrosis, and oncogenesis in MASH-HCC, offering a potential target for therapeutic intervention. - Source: PubMed
Publication date: 2024/04/01
Srinivas Akshatha NSuresh DiwakarVishwanath Prashant MSatish SuchithaSanthekadur Prasanna KKoka SaisudhaKumar Divya P - Frequent drought events due to climate change have become a major threat to maize (Zea mays L.) production and food security in Africa. Genetic engineering is one of the ways of improving drought tolerance through gene introgression to reduce the impact of drought stress in maize production. This study aimed to evaluate the efficacy of Event MON 87460 (CspB; DroughtGard®) gene in more than 120 conventional drought-tolerant maize hybrids in Kenya, South Africa, and Uganda for 3-6 years under managed drought-stress and optimal conditions and establish any additional yield contribution or yield penalties of the gene in traited hybrids relative to their non-traited isohybrids. Germplasm used in the study were either MON 87460 traited un-adapted (2008-2010), adapted traited DroughtTEGO® (2011-2013) or a mix of both under confined field trials. - Source: PubMed
Publication date: 2024/02/01
Obunyali Caleb OPillay KiruMeisel BarbaraNdou Eric NMashingaidze KingstoneSserumaga Julius PytonAsea GodfreyMwimali MurengaTende ReginaBeyene YosephMugo StephenOkogbenin EmmanuelOikeh Sylvester O - Green Care therapies are defined as the engagement of a patient with the nature, exposing patients to a nature based therapeutic setting that may facilitate their recovery. Such therapies became popular at the end of the twentieth century. This therapeutic approach may include therapeutic horticulture, nature therapies, care farming, facilitated exercise, and animal-assisted therapies with farm animals (AATF). This paper describes the processes of planning and creating an AATF-based clinical intervention wherein persons with TBI interacted with ducks (in twice weekly, 1-hour groups) for 12 wk at a TBI rehabilitation facility. The discussion includes site identification, stakeholder engagement, intervention design and human and animal safety procedures. The research methods, theoretical framework, ethical consideration, and risk reduction strategies for human participants and ducks are discussed. Also, description of challenges and blueprints of possible solutions for other researchers interested in developing similar initiatives. This program will serve as a study site for examining effects of AATF-based interventions on self-efficacy, depression, and anxiety in persons with TBI. If the study suggests that AATF interventions with ducks may lead to positive changes, the proposed study will be followed with studies that include larger samples at multiple sites. Findings in this paper may contribute to the implementation science body of knowledge. Because of that, the information in this paper may benefit the researchers outside of the healthcare arena. From that perspective methods described in this paper may help to develop studies that focus on policy development, program expansion, or individual project implementation. - Source: PubMed
Publication date: 2024/01/17
Sargsyan AlexBeebe Lora H - We present prenatal diagnosis and perinatal findings of 17q12 microdeletion encompassing HNF1B in a fetus with bilateral hyperechogenic kidneys on fetal ultrasound and mild renal abnormality after birth, and a review of the literature. - Source: PubMed
Chen Chih-PingWu Fang-TzuPan Yen-TingWu Peih-ShanWang Wayseen - Genetic kidney diseases are underdiagnosed; namely, from 7% to 40% of patients suffering from chronic kidney disease (CKD) can carry a pathogenic variant, depending on population characteristics. Hereditary tubulointerstitial kidney diseases, including autosomal dominant tubulointerstitial kidney diseases (ADTKD), are even more challenging to diagnose. ADTKD is a rare form of genetic kidney disease resulting from pathogenic variants in the and genes. There is no typical clinical or histopathological sign of ADTKD, it is characterized by progressive CKD, an autosomal dominant inheritance pattern, and tubular atrophy with interstitial fibrosis on kidney biopsy. There is no significant proteinuria, and the urinary sediment is bland. The patients usually do not have severe arterial hypertension. There can be a history of early gout, especially when compared to the UMOD gene variants. Children can have enuresis due to a loss of renal concentration. On ultrasound, the kidneys can appear normal or small in size. Renal cysts are not pathognomonic for any of the named diseases. End-stage renal disease (ESRD) develops at the average age of 45, but this can be very variable. Family history that suggests autosomal dominant inheritance and CKD fulfilling the aforementioned characteristics of tubulointerstitial kidney disease should raise suspicion of ADTKD. In the setting of a negative family history for CKD, clinical suspicion should be raised based on clinical characteristics, including early onset of hyperuricemia or gout and compatible histology on the kidney biopsy. Contrary to the aforementioned characteristics of ADTKD, in the case of HNF1B-related disease, there is a more complex clinical presentation with extrarenal manifestations of the disease (diabetes mellitus, hypomagnesemia, neurologic and psychiatric disturbances, etc.). The diagnosis of ADTKD is based on a positive family history and a detection of the pathogenic variant in one of the genes in an affected individual. - Source: PubMed
Publication date: 2023/11/10
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