RAIDD (Intermediate Domain) Peptide
- Known as:
- RAIDD (Intermediate Domain) Peptide
- Catalog number:
- 1115P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- RAIDD (Intermediate Domain) Peptide
Related genes to: RAIDD (Intermediate Domain) Peptide
- Gene:
- CRADD NIH gene
- Name:
- CASP2 and RIPK1 domain containing adaptor with death domain
- Previous symbol:
- -
- Synonyms:
- RAIDD
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2016-01-15
Related products to: RAIDD (Intermediate Domain) Peptide
α - Calcitonin Gene Related Peptide, α - CGRP, rat&_945;2&_946;1 Integrin Ligand Peptide&_946;_catenin peptide(1S,2R,3S,5R)_3_(phenymethyloxy)_2_(p Entecavir Intermediate I(1S,2S,3S,5S)_5_(2_Amino_6_(benzyloxy) Entecavir Intermediate I(2R,3S,5S)_3_(benzyloxy)_5_(6_benzyloxy Entecavir Intermediate(4R)_cis_6_1,1_Dimethyl_6_cyanomethyl_2 ATS_8 ; Intermediate of(Ala92)-Peptide 6 98% C93H155N31O26 CAS:(Arg)9 Peptide (Arg8)-Vasopressin Biotin peptide This is (Arg8)-Vasopressin Biotin peptide. For research use only.(Asn5)-Delta-Sleep Inducing Peptide
(Asn5)-Delta-Sleep Inducing Peptide (rabbit), (Asn5)-DSIP (rabbit) 98% C35H49N11O14 CAS: 80064-67-1(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Biotin Conjugates) Dopamine D2 Receptor Immunogen: peptide Host: Rabbit(Biotin Conjugates) Glucose Transporter 1 Immunogen: peptide Host: Rabbit Related articles to: RAIDD (Intermediate Domain) Peptide
- Prostate cancer is a significant global health concern that requires innovative therapeutic investigations. Here, the potential anticancer properties of tannic acid were evaluated by examining its effects on apoptosis in prostate cancer cell lines. PC-3 and LnCaP prostate adeno carcinoma cells, along with PNT1A prostate control cells, were cultured and divided into untreated and tannic acid-treated groups. Cell proliferation, cytotoxicity, and effects of tannic acid on the cell death mechanism were evaluated. mRNA expression levels of 84 genes were explored in cells following tannic acid treatment. Notably, tannic acid-induced down-regulation of several pro-survival genes, including and in both cell lines. Moreover, tannic acid treatment led to the up-regulation of various pro-apoptotic genes, such as in both PC-3 and LnCap cells. These findings highlight tannic acid's ability to induce apoptosis in prostate cancer cells through pro-apoptotic pathways. This study concludes that tannic acid selectively inhibits prostate cancer cell growth. - Source: PubMed
Publication date: 2024/09/14
Kandir SinanKarakurt SevtapGökçek-Saraç ÇiğdemKarakurt Serdar - Caspase 9 (CASP9) is a well-known initiator caspase of intrinsic apoptosis. In humans, cIAP1 binds and induces degradation of the activated form of CASP9, but not pro-CASP9. In fish, the activity and regulation of CASP9 remain unknown. In this work, using flounder Paralichthys olivaceus as a representative species, we examined the regulatory mechanism of CASP9 in teleost. P. olivaceus CASP9 (PoCASP9) induced robust apoptosis, which was inhibited by P. olivaceus cIAP1 (PocIAP1). Unlike human cIAP1, PocIAP1 bound both pro- and active PoCASP9 and induced their degradation via the RING domain-involved proteasome pathway. In humans, the adaptor molecule CRADD cannot interact with CASP9. In contrast, P. olivaceus CRADD (PoCRADD) bound both pro- and active PoCASP9 via CARD-CARD interaction and enhanced apoptosis by promoting the cellular levels of pro- and active PoCASP9. Furthermore, PoCRADD abrogated the inhibition of PoCASP9 by PocIAP1 by preventing PocIAP1-PoCASP9 interaction. Together these results reveal a CASP9 regulation mechanism in teleost that differs from that in humans and demonstrate that teleost CASP9 is tightly and directly controlled by both negative and positive regulators that exert a regulation effect both before and after CASP9 activation. These findings advance our understanding of the regulation of CASP9-mediated apoptosis in vertebrates. - Source: PubMed
Publication date: 2024/09/02
Wu MengChen YuanYuan ZihaoXu HangSun Li - Quantitative real-time PCR (qRT-PCR) has been widely employed for the study of gene expression in fish, and accurate normalization is crucial. In this study, we aimed to identify the most stably expressed genes in various tissues, different developmental stages, and within astaxanthin treatment groups in Lutjanus erythropterus. Twelve candidate genes (EEF1A, CYB5R3, DLD, IDH3A, MRPL17, MRPL43, NDUFS7, PABPC1, PAGR1, PFDN2, PSMC3, and RAB10) were examined via qRT-PCR. We employed geNorm and NormFinder to assess their stability. The results revealed that RAB10 and PFDN2 exhibited relatively stable expression patterns across different tissue and astaxanthin treatment groups, while NDUFS7 and MRPL17 proved to be the most reliable reference gene combinations across various developmental stages. The stability of these selected genes was further validated by assessing the expression of two target genes, CRADD and CAPNS1, across developmental stages, reinforcing the reliability of NDUFS7 as it closely aligned with transcriptome-wide expression patterns at these stages. The present results will help researchers to obtain more accurate results in future qRT-PCR analysis in L. erythropterus. - Source: PubMed
Publication date: 2024/06/10
Chen LujunLiang QiuluLai ZhuoxinCui HaitaoXu ZhenminChen ZizhaoDong ZhongdianWang ZhongduoGuo Yusong - Depression is a major global burden with unclear pathophysiology and poor treatment outcomes. Diagnosis of depression continues to rely primarily on behavioral rather than biological methods. Investigating tools that might aid in diagnosing and treating early-onset depression is essential for improving the prognosis of the disease course. While there is increasing evidence of possible biomarkers in adult depression, studies investigating this subject in adolescents are lacking. - Source: PubMed
Publication date: 2024/05/15
Sokolov Aleksandr VLafta Muataz SNordberg Didi O TJonsson JörgenSchiöth Helgi B - Deregulated centrosome numbers are frequently found in human cancer and can promote malignancies in model organisms. Current research aims to clarify if extra centrosomes are cause or consequence of malignant transformation, and if their biogenesis can be targeted for therapy. Here, we show that oncogene-driven blood cancer is inert to genetic manipulation of centrosome numbers, whereas the formation of DNA damage-induced malignancies is delayed. We provide first evidence that this unexpected phenomenon is connected to extra centrosomes eliciting a pro-death signal engaging the apoptotic machinery. Apoptosis induction requires the PIDDosome multi-protein complex, as it can be abrogated by loss of any of its three components, , , or . BCL2 overexpression equally blocks cell death, documenting for the first time induction of mitochondrial apoptosis downstream of extra centrosomes. Our findings demonstrate context-dependent effects of centrosome amplification during transformation and ask to adjust current belief that extra centrosomes are intrinsically pro-tumorigenic. - Source: PubMed
Publication date: 2024/03/29
Braun Vincent ZKarbon GerlindeSchuler FabianSchapfl Marina AWeiss Johannes GPetermann Paul YSpierings Diana C JTijhuis Andrea EFoijer FlorisLabi VerenaVillunger Andreas