FKBP1A _ FKBP12 Antibody
- Known as:
- FKBP1A _ FKBP12 Antibody
- Catalog number:
- 10268-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- FKBP1A _ FKBP12 Antibody
Related genes to: FKBP1A _ FKBP12 Antibody
- Gene:
- FKBP1A NIH gene
- Name:
- FKBP prolyl isomerase 1A
- Previous symbol:
- FKBP1
- Synonyms:
- FKBP-12, FKBP12, PKC12, PPIASE, FKBP12C
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-14
- Date modifiied:
- 2018-11-01
- Gene:
- FKBP1B NIH gene
- Name:
- FKBP prolyl isomerase 1B
- Previous symbol:
- FKBP1L
- Synonyms:
- OTK4, FKBP12.6, PPIase, FKBP9
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-15
- Date modifiied:
- 2018-11-01
Related products to: FKBP1A _ FKBP12 Antibody
Related articles to: FKBP1A _ FKBP12 Antibody
- Dogs are the only large mammals, besides humans, that develop spontaneous prostate cancer, which has a poor prognosis and limited treatment efficacy. Considering the central role of mammalian target of rapamycin (mTOR) in carcinogenesis, the use of rapamycin, an mTOR inhibitor, has attracted considerable attention. In this study, we performed gene expression microarray analyses of normal canine prostate and prostate carcinoma cells. Among the 6,270 differentially expressed genes revealed in the transcriptome, 3,242 were upregulated and 3,028 were downregulated, and were related to phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR pathway activation, as confirmed by enrichment analysis. Among the genes involved in this pathway, we found increased expression levels of FKBP1A, FKBP1B, AKT1S1, PDK2, PIP5K1 and PIP5KL1 in canine prostate cancer cells compared with normal prostate cells. We also treated two canine prostate cancer cell lines (PC1 and PC2) with rapamycin in vitro (6, 10 and 12 μM) for 24 h and observed a dose-dependent decrease in cell viability. Our results indicate that rapamycin significantly increased AKT transcript levels in both cell lines, indicating resistance to treatment. However, mTOR and 4E-BP1 expression were downregulated after rapamycin treatment. We suggest that mTOR inhibition is a potential treatment of choice for canine prostate cancer, which may guide and contribute to future prostate carcinoma clinical trials. However, the acquisition of resistance to treatment remains a challenge, and precision medicine may help overcome this problem. - Source: PubMed
Publication date: 2025/05/05
Kobayashi Priscila ELainetti Patrícia FLeis-Filho Antonio FDelella Flávia KVicente Igor S TFonseca-Alves Carlos ELaufer-Amorim Renée - Autophagy played a crucial regulatory role in tumor initiation and progression. Therefore, we aimed to comprehensively analyze autophagy-related genes (ARGs) in gastric cancer, focusing on their expression, prognostic value, and potential functions. - Source: PubMed
Publication date: 2024/03/25
Yin YichenWang BaozhenYang MingzheChen JingLi Tao - Current disease-modifying therapies for Huntington disease (HD) focus on lowering mutant HTT (huntingtin; mHTT) levels, and the immunosuppressant drug rapamycin is an intriguing therapeutic for aging and neurological disorders. Rapamycin interacts with FKBP1A/FKBP12 and FKBP5/FKBP51, inhibiting the MTORC1 complex and increasing cellular clearance mechanisms. Whether the levels of FKBP (FK506 binding protein) family members are altered in HD models and if these proteins are potential therapeutic targets for HD have not been investigated. Here, we found levels of FKBP5 are significantly reduced in HD R6/2 and zQ175 mouse models and human HD isogenic neural stem cells and medium spiny neurons derived from induced pluripotent stem cells. Moreover, FKBP5 interacts and colocalizes with HTT in the striatum and cortex of zQ175 mice and controls. Importantly, when we decreased FKBP5 levels or activity by genetic or pharmacological approaches, we observed reduced levels of mHTT in our isogenic human HD stem cell model. Decreasing FKBP5 levels by siRNA or pharmacological inhibition increased LC3-II levels and macroautophagic/autophagic flux, suggesting autophagic cellular clearance mechanisms are responsible for mHTT lowering. Unlike rapamycin, the effect of pharmacological inhibition with SAFit2, an inhibitor of FKBP5, is MTOR independent. Further, treatment for 2 weeks with SAFit2, results in reduced HTT levels in both HD R6/2 and zQ175 mouse models. Our studies establish FKBP5 as a protein involved in the pathogenesis of HD and identify FKBP5 as a potential therapeutic target for HD. : ACTB/β-actin: actin beta; AD: Alzheimer disease; BafA1: bafilomycin A; BCA: bicinchoninic acid; BBB: blood brain barrier; BSA: bovine serum albumin; CoIP: co-immunoprecipitation; DMSO: dimethyl sulfoxide; DTT: dithiothreitol; FKBPs: FK506 binding proteins; HD: Huntington disease; HTT: huntingtin; iPSC: induced pluripotent stem cells; MAP1LC3/LC3:microtubule associated protein 1 light chain 3; MAPT/tau: microtubule associated protein tau; MES: 2-ethanesulfonic acid; MOPS: 3-(N-morphorlino)propanesulfonic acid); MSN: medium spiny neurons; mHTT: mutant huntingtin; MTOR: mechanistic target of rapamycin kinase; NSC: neural stem cells; ON: overnight; PD: Parkinson disease; PPIase: peptidyl-prolyl -isomerases; polyQ: polyglutamine; PPP1R1B/DARPP-32: protein phosphatase 1 regulatory inhibitor subunit 1B; PTSD: post-traumatic stress disorder; RT: room temperature; SQSTM1/p62: sequestosome 1; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; TBST:Tris-buffered saline, 0.1% Tween 20; TUBA: tubulin; ULK1: unc-51 like autophagy activating kinase 1; VCL: vinculin; WT: littermate controls. - Source: PubMed
Publication date: 2021/05/24
Bailus Barbara JScheeler Stephen MSimons JesseSanchez Maria ATshilenge Kizito-TshitokoCreus-Muncunill JordiNaphade SwatiLopez-Ramirez AlejandroZhang NingzheLakshika Madushani KuruwitageMoroz StanislavLoureiro AshleySchreiber Katherine HHausch FelixKennedy Brian KEhrlich Michelle EEllerby Lisa M - The heterogeneity of colorectal cancer (CRC) poses a significant challenge to the precise treatment of patients. CRC has been divided into 4 consensus molecular subtypes (CMSs) with distinct biological and clinical characteristics, of which CMS4 has the mesenchymal identity and the highest relapse rate. Autophagy plays a vital role in CRC development and therapeutic response. - Source: PubMed
Wang LiangbinJiang XinleiZhang XingguoShu Peng - Genetic and epigenetics factors have been implicated in drug response, graft function and rejection in solid organ transplantation. Differential expression of genes involved in calcineurin and mTOR signaling pathway and regulatory miRNAs was analyzed in the peripheral blood of kidney recipient cohort (n=36) under tacrolimus-based therapy. - Source: PubMed
Bonezi VivianGenvigir Fabiana Dalla VecchiaSalgado Patrícia de CássiaFelipe Claudia RossoTedesco-Silva HelioMedina-Pestana José OsmarCerda AlvaroDoi Sonia QuateliHirata Mario HiroyukiHirata Rosario Dominguez Crespo