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Mouse Anti-PRDM1 Recombinant Antibody (CBYC-P587) (CBMAB-P2696-YC)

Provided herein is a Mouse monoclonal antibody against Human PR/SET Domain 1. The antibody can be used for immunoassay techniques, such as ELISA, WB.
See all PRDM1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYC-P587
Antibody Isotype
IgG2b, κ
Application
ELISA, WB

Basic Information

Immunogen
PRDM1 (NP_001189, 422-493 aa) full length recombinant protein with GST tag.
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
PBS, pH 7.2
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
PRDM1
Introduction
PRDM1 is a protein that acts as a repressor of beta-interferon gene expression. The protein binds specifically to the PRDI (positive regulatory domain I element) of the beta-IFN gene promoter. Transcription of this gene increases upon virus induction.
Entrez Gene ID
UniProt ID
Alternative Names
BLIMP1; PRDI-BF1
Function
Transcription factor that mediates a transcriptional program in various innate and adaptive immune tissue-resident lymphocyte T cell types such as tissue-resident memory T (Trm), natural killer (trNK) and natural killer T (NKT) cells and negatively regulates gene expression of proteins that promote the egress of tissue-resident T-cell populations from non-lymphoid organs. Plays a role in the development, retention and long-term establishment of adaptive and innate tissue-resident lymphocyte T cell types in non-lymphoid organs, such as the skin and gut, but also in other nonbarrier tissues like liver and kidney, and therefore may provide immediate immunological protection against reactivating infections or viral reinfection (By similarity).
Binds specifically to the PRDI element in the promoter of the beta-interferon gene (PubMed:1851123).
Drives the maturation of B-lymphocytes into Ig secreting cells (PubMed:12626569).
Associates with the transcriptional repressor ZNF683 to chromatin at gene promoter regions (By similarity).
Biological Process
Adaptive immune responseIEA:UniProtKB-KW
Aorta developmentIEA:Ensembl
Artery morphogenesisIEA:Ensembl
Cell fate commitmentManual Assertion Based On ExperimentIBA:GO_Central
Coronary vasculature developmentIEA:Ensembl
Eye photoreceptor cell developmentIEA:Ensembl
Gene expressionIEA:Ensembl
Germ cell developmentIEA:Ensembl
Heart valve developmentIEA:Ensembl
Histone arginine methylationIEA:Ensembl
Innate immune responseIEA:UniProtKB-KW
Intestinal epithelial cell developmentIEA:Ensembl
Kidney developmentIEA:Ensembl
Maternal placenta developmentIEA:Ensembl
Morphogenesis of a branching structureIEA:Ensembl
Negative regulation of gene expressionIEA:Ensembl
Negative regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:NTNU_SB
Positive regulation of gene expressionIEA:Ensembl
Post-embryonic developmentIEA:Ensembl
Regulation of cell population proliferationIEA:Ensembl
Regulation of extrathymic T cell differentiationISS:UniProtKB
Regulation of gene expressionManual Assertion Based On ExperimentIBA:GO_Central
Regulation of natural killer cell differentiationISS:UniProtKB
Regulation of NK T cell differentiationISS:UniProtKB
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Response to radiationIEA:Ensembl
Sebum secreting cell proliferationIEA:Ensembl
Trophoblast giant cell differentiationIEA:Ensembl
Ventricular septum developmentIEA:Ensembl
Cellular Location
Nucleus
Cytoplasm
Involvement in disease
In certain aggressive cases of activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL), PRDM1 protein instability has been observed. This instability, which impairs B-cell differentiation, is caused by N-terminal misfolding mutations, including those occurring at positions Pro-84 and Ile-107, and results in PRDM1 protein sequestration in the cytoplasm, followed by proteasomal degradation via a heat shock protein 70 HSPA1A-SYNV1/HRD1 pathway. These N-terminal mutations do not affect PRDM1 transcription regulation activity. HSPA1A inhibition restores PRDM1 nuclear localization and transcriptional activity in lymphoma cell lines and suppresses tumor growth in xenografts, more efficiently than proteasome inhibition.
PTM
Sumoylation at Lys-816 by PIAS1 augments transcriptional repressor activity, and is critical for plasma cell differentiation (PubMed:22555612).
Can be sumoylated with SUMO1 and SUMO2 by PML. Degradation of the wild-type protein mostly depends upon sumoylation, rather than ubiquitination (PubMed:28842558).
Desumoylated by SENP1 and SENP6 (PubMed:28842558).
Ubiquitinated by the SCF(FBXO11) complex, leading to its degradation by the proteasome.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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