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anti-Human Cullin 1 Antibodies:
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Human Polyclonal Cullin 1 Primary Antibody for IF, IHC - ABIN6241499
Mao, Xiong, Huang, Zheng, Yao: Expression of CUL1 correlates with tumour-grade and recurrence in urothelial carcinoma. in ANZ journal of surgery 2018
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Human Polyclonal Cullin 1 Primary Antibody for IHC, WB - ABIN3015864
Chen, Xu, Yang, Zhang, Wu, Chen, Li, Wang, Li, Li, Dai: Upregulation of miR-223 in the rat liver inhibits proliferation of hepatocytes under simulated microgravity. in Experimental & molecular medicine 2018
Show all 2 Pubmed References
Human Polyclonal Cullin 1 Primary Antibody for IHC, WB - ABIN6669899
Liao, Jiang, He, Ni, Tu, Zhang, Wang, Lou, Quan, Wang: NEDD8-mediated neddylation is required for human endometrial stromal proliferation and decidualization. in Human reproduction (Oxford, England) 2016
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Human Polyclonal Cullin 1 Primary Antibody for WB - ABIN1537543
Jiang, He, Xu, Liu, Qu, Tong: Cullin-1 promotes cell proliferation via cell cycle regulation and is a novel in prostate cancer. in International journal of clinical and experimental pathology 2015
Human Polyclonal Cullin 1 Primary Antibody for IF, IHC - ABIN6711720
Liu, Yang, Zhao, Zhang, Song, Hu: NEDD8 ultimate buster-1 long (NUB1L) protein promotes transfer of NEDD8 to proteasome for degradation through the P97UFD1/NPL4 complex. in The Journal of biological chemistry 2013
High expression of CUL1 is associated with colorectal cancer.
we analyzed eight probands with clinically suspected Weaver syndrome by whole-exome sequencing and identified three mutations: a 25.4-kb deletion partially involving EZH2 and CUL1 ,a missense mutation , and a missense mutation in SUZ12 inherited from her father .In vitro functional analyses demonstrated that the identified EED and SUZ12 missense mutations cause decreased decreased trimethylation of lysine 27 of H3
DCUN1D3 has a role in activating SCFSKP2 ubiquitin E3 ligase activity through cullin-1 neddylation and cell cycle progression in tumor cells with UV damage
Cullin1 and MMP-2 expressions could be novel diagnostic and prognostic markers for colorectal cancer patients.
Our results demonstrate that increased CUL1 expression is significantly correlated with poor prognosis of patients with osteosarcoma. CUL1 might be an important marker and a therapeutic target for osteosarcoma.
Our results demonstrate that increased CUL1 expression is significantly correlated with poor prognosis of patients with urothelial carcinoma
unneddylated Cul1 is another central player involved in maintenance of the adaptor module pool through the formation of Cul1-Skp-1-F-box complexes and promotion of rapid SCF assembly
Data suggest that cullin1 (Cul1) may constitute a potential therapeutic target in renal cell carcinoma (RCC).
Cul1 promoted mTORC1 activity and cap-dependent translation by enhancing the ubiquitination and degradation of DEPTOR. eIF4F suppression inhibited the promoting effect of Cul1 on melanoma cell proliferation.
Data show that melanoma antigen, family C, 2 protein (MAGE-C2) binds with RING-box protein 1 (Rbx1) and Cullin 1, and regulates cyclin E stability in melanoma cells.
High Cul1 expression predicts worse 5-year overall and disease-specific survival rates in HCC patients.
Nedd8(Q40E) cannot induce the same structural effect on Cul1-Rbx1 as wild-type Nedd8.
Cullin-1 has been deeply implicated in the pathogenesis and development of prostate cancer
Increased CUL1 expression in CRC cells significantly promoted cell migration and invasion abilities in vitro and peritoneal metastasis in vivo through inducing high expression of MMPs.
Our data indicated that Cul1 expression significantly increased in human glioma, and it may be involved in proliferation, migration and invasion of glioma cells.
In papillary thyroid carcinoma, cytoplasmic expression of Cul1 was correlated with tumor occurrence, N stage and Cyclin D1 expression. Nuclear Cul1 expression was negatively correlated with tumor occurence.
We discuss how these results can explain the rapid association of Cdc34 and SCF.
By integrating our WES and CN data we identified three mutated putative candidate genes targeted by 7q deletions (CUL1, EZH2 and FLNC), with FLNC positioned within the well-characterized 7q minimally deleted region.
Integrative analysis of mutations and somatic copy-number alterations revealed frequent genetic alterations in BAP1, NF2, CDKN2A, and CUL1 in pleural mesothelioma.
data suggested that Cullin1 might promote the progression of non-small-cell lung cancer
Cul-1 deneddylation led to Deptor accumulation and subsequent mTOR inactivation, which had an inhibitory effect on dendritic cells in mouse model of inflammatory bowel disease.
Lysine 29-linkage of ASK1 by Skp1-Cullin 1-Fbxo21 ubiquitin ligase complex is required for antiviral innate response.
Substrate binding promotes formation of the Skp1-Cul1-Fbxl3 (SCF(Fbxl3)) protein complex.
Rictor forms a complex with Cullin-1 to promote SGK1 ubiquitination and destruction.
Skp2 and Cul1 expression is repressed by GATA2, thereby inhibiting ubiquitin/proteasome-dependent degradation of p21(WAF1) and p27(Kip1), inducing their accumulation, and suppressing hematopoietic stem cell growth
Analysis of cell cycle regulatory genes reveals defective induction of the c-Myc:CUL1 ubiquitin ligase pathway in B cells from CD22-deficient mice in the context of a C57BL/6 genetic background, following IgM ligation compared with wild-type B cells.
Cul7 forms a heterodimeric complex with Cul1 in a manner dependent on Fbxw8.
SCCRO recruits Ubc12 approximately NEDD8 to the CAND1-Cul1-ROC1 complex but that this is not sufficient to dissociate or overcome the inhibitory effects of CAND1 on cullin neddylation
Results show that Cullin-1-mediated protein degradation plays an essential role in the correct allocation of neural crest fates during embryogenesis.
The SCF-complex gene expression has been characterized during bovine preimplantation development.
Around the time of major gene activation, expression of cullin 1 switches from transcript variant 1 to transcript variant 3.
ALF4 binds to RBX1 and inhibits the activity of SCF(TIR)(1), an E3 ligase responsible for degradation of the Aux/IAA transcriptional repressors. In vivo, the alf4 mutation destabilizes the CUL1 subunit of the SCF
The axr6-101 phenotype is caused by the E716K substitution of the CUL1 protein, which is likely to affect its ability to bind to the C-terminal RING domain of RING-box 1 (RBX1).
a new viable recessive allele of the Arabidopsis CULLIN1 gene in the non-reference Wassilewskija (Ws-4) accession, was identified.
icu13 is a novel recessive allele of AUXIN RESISTANT6 (AXR6), which encodes CULLIN1, an invariable component of the SCF complex.[ICU13] [ncurvata13]
Genetic and physiological data to directly demonstrate that AtCUL1 is necessary for normal JA responses are presented.
A viable and fertile weak allele of CUL1, called cul1-6, is described.
CUL1 is required for TOC1 degradation and suggests that this protein is the functional cullin circadian clock.
The disruption of the CAND1-CUL1 interaction results in an increased abundance of assembled SCF(TIR1) complex; stabilization of the CAND1-CUL1 interaction diminishes SCF(TIR1) complex abundance.
the first reported allele of CUL1 to directly affect subunit interactions at the CUL1 C terminus
CUL1-based SCF E3 ligase activity is required for Della protein degradation.
Core component of multiple cullin-RING-based SCF (SKP1- CUL1-F-box protein) E3 ubiquitin-protein ligase complexes, which mediate the ubiquitination of proteins involved in cell cycle progression, signal transduction and transcription. In the SCF complex, serves as a rigid scaffold that organizes the SKP1-F-box protein and RBX1 subunits. May contribute to catalysis through positioning of the substrate and the ubiquitin-conjugating enzyme. The E3 ubiquitin-protein ligase activity of the complex is dependent on the neddylation of the cullin subunit and is inhibited by the association of the deneddylated cullin subunit with TIP120A/CAND1. The functional specificity of the SCF complex depends on the F-box protein as substrate recognition component. SCF(BTRC) and SCF(FBXW11) direct ubiquitination of CTNNB1 and participate in Wnt signaling. SCF(FBXW11) directs ubiquitination of phosphorylated NFKBIA. SCF(BTRC) directs ubiquitination of NFKBIB, NFKBIE, ATF4, SMAD3, SMAD4, CDC25A, FBXO5 and probably NFKB2. SCF(SKP2) directs ubiquitination of phosphorylated CDKN1B/p27kip and is involved in regulation of G1/S transition. SCF(SKP2) directs ubiquitination of ORC1, CDT1, RBL2, ELF4, CDKN1A, RAG2, FOXO1A, and probably MYC and TAL1. SCF(FBXW7) directs ubiquitination of cyclin E, NOTCH1 released notch intracellular domain (NICD), and probably PSEN1. SCF(FBXW2) directs ubiquitination of GCM1. SCF(FBXO32) directs ubiquitination of MYOD1. SCF(FBXO7) directs ubiquitination of BIRC2 and DLGAP5. SCF(FBXO33) directs ubiquitination of YBX1. SCF(FBXO11) does not seem to direct ubiquitination of TP53. SCF(BTRC) mediates the ubiquitination of NFKBIA at 'Lys-21' and 'Lys-22'\; the degradation frees the associated NFKB1-RELA dimer to translocate into the nucleus and to activate transcription. SCF(Cyclin F) directs ubiquitination of CP110 (By similarity).
, Cell division control 53 homolog