Rat Anti-AICDA Recombinant Antibody (V2-180327) (CBMAB-A1784-YC)

Name: Rat Anti-AICDA Recombinant Antibody (V2-180327)
SKU: CBMAB-A1784-YC
Rating: 5 (1 reviews)

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Published Data

Rat Anti-AICDA Recombinant Antibody (EK2-5G9) (CBMAB-A1784-YC) in WB

BCL6 protein levels were measured in 4WT and 4AIDKO, 10AIDKO and 19AIDKO cells by immunoblots, and GAPDH protein was taken as an internal control. ...View More

Jiao, J., Lv, Z., Zhang, P., Wang, Y., Yuan, M., Yu, X., ... & Ji, Y. (2020). AID assists DNMT1 to attenuate BCL6 expression through DNA methylation in diffuse large B-cell lymphoma cell lines. Neoplasia, 22(3), 142-153.

Rat Anti-AICDA Recombinant Antibody (EK2-5G9) (CBMAB-A1784-YC) in IHC

Representative results of p53, Fhit, E-cadherin and AID immunostaining in HPSCC tissue. (A) Positive p53 immunostaining of CIS in hypopharyngeal cancer. (B) Reduced Fhit immunostaining of CIS and positive staining of the germinal center and infiltrating lymphocytes. (C) Reduced E-cadherin immunostaining of CIS and decreased membrane staining of E-cadherin in <30% of the tumor cells. (D) Positive AID immunostaining of CIS in hypopharyngeal cancer. Scale bar, 200 µm. Magnification, ×200. Fhit, Fragile Histidine Triad; AID, activation-induced cytidine deaminase; HPSCC, hypopharyngeal squamous cell carcinoma; CIS, carcinoma in situ. ...View More

Yamamoto, S., Yashima, K., Kawata, S., Hosoda, K., Tamoto, A., Ikebuchi, Y., ... & Isomoto, H. (2017). Frequent aberrant p53 and Fhit expression in endoscopically resected superficial hypopharyngeal cancer and esophageal cancer. Oncology Letters, 14(1), 587-592.

Rat Anti-AICDA Recombinant Antibody (EK2-5G9) (CBMAB-A1784-YC) in IF

Tertiary lymphoid tissues (TLTs) form in aged human kidneys.
(A-L) Histological analyses of aged human kidney samples. (A and B) Periodic acid-Schiff (PAS) staining and immunofluorescence analysis of (C) CD20 and CD3ε; (E) Ki67 and CD3ε/CD20 (arrowheads indicate double-positive cells); (G) CXCL13 and CD21; (J) CXCL13 and CD45; (K) CD21, α-smooth muscle actin (αSMA), and CD45; and (L) p75 neurotrophin receptor (p75NTR) and CD21, and immunohistochemical analysis of (D) peripheral lymph node addressin (PNAd); (F) CD21 (arrowheads indicate the localization of CD21+ follicular dendritic cell [FDC] networks); (H) CD20, activation-induced cytidine deaminase (AID), CD21, and retinaldehyde dehydrogenase 2 (RALDH2) (serial sections); and (I) RALDH2 (arrowheads indicate the localization of B cell follicles). The outlined region in (H) is magnified in (I). Arrows indicate TLT localization. Scale bars: (A, D, H, K, and L) 50 μm, (B, C, and F) 100 μm, (E, G, I, and J) 10 μm. (M) Quantitative analysis of TLT frequencies in human samples. ...View More

Sato, Y., Mii, A., Hamazaki, Y., Fujita, H., Nakata, H., Masuda, K., ... & Yanagita, M. (2016). Heterogeneous fibroblasts underlie age-dependent tertiary lymphoid tissues in the kidney. JCI insight, 1(11).

Rat Anti-AICDA Recombinant Antibody (EK2-5G9) (CBMAB-A1784-YC) in FC and WB

B cell lineage-specific activation of AID in BCR-ABL1-transformed leukemia cells
(A) Quantitative RT-PCR analysis of AID mRNA expression in CD13− CD19+ B lymphoid (CML-LBC) and CD13+ CD19− myeloid (CML-CP) bone marrow cells sorted from four patients (I-IV) with early B lymphoid blast crisis CML. Peripheral blood naïve (IgD+) and germinal center (GC) B cells were used as negative and positive controls, respectively. AID mRNA levels (means ± SD) were normalized based on COX6B transcripts. (B) AID protein levels in CML-LBC and CML-CP cells from two patients (I-II) were compared to those of tonsillar GC B cells by Western blotting using EIF4E as loading control. (C) PAX5 mRNA levels in sorted CML-CP and CML-LBC cells were measured by quantitative RT-PCR (means + SD). (D) AID protein expression in chronic phase and lymphoid blast crisis CML cells (I-IV) was measured by flow cytometry (intracellular staining) using diffuse large B cell lymphoma (DLBCL) cells as control. (E) Bone marrow cells from AID-GFP reporter transgenic mice were transduced with BCR-ABL1 or empty vector control and cultured under myeloid (IL3, IL6, SCF) or B lymphoid (IL7) growth conditions. (F) AID mRNA levels (means ± SD) in sorted GFP− (gray) and GFP+ (green) cell populations from LPS/IL4-stimulated splenic B cells or BCR-ABL1-transformed leukemia cells from AID-GFP transgenic mice were measured by quantitative RT-PCR. ...View More

The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia

Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Rat

Clone

V2-180327

Application

ELISA, IHC-F, IHC-P, WB

Immunogen

Synthetic peptide corresponding to amino acids 185-198 of human AICDA

Host Species

Rat

Specificity

Human

Antibody Isotype

IgG2b

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, 0.09% sodium azide

Buffer

PBS

Preservative

< 0.1% sodium azide

Concentration

1 mg/ml

Storage

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

More Infomation

Target

Full Name

Activation Induced Cytidine Deaminase

Introduction

AICDA is a RNA-editing deaminase that is a member of the cytidine deaminase family. The protein is involved in somatic hypermutation, gene conversion, and class-switch recombination of immunoglobulin genes. Defects in this gene are the cause of autosomal

Entrez Gene ID

57379

UniProt ID

Q9GZX7

Alternative Names

Activation Induced Cytidine Deaminase; Activation-Induced Cytidine Deaminase; Cytidine Aminohydrolase; AID; Integrated Into Burkitts Lymphoma Cell Line Ramos; Single-Stranded DNA Cytosine Deaminase; Epididymis Secretory Protein Li 284;

Function

Single-stranded DNA-specific cytidine deaminase. Involved in somatic hypermutation (SHM), gene conversion, and class-switch recombination (CSR) in B-lymphocytes by deaminating C to U during transcription of Ig-variable (V) and Ig-switch (S) region DNA. Required for several crucial steps of B-cell terminal differentiation necessary for efficient antibody responses (PubMed:18722174, PubMed:21385873, PubMed:21518874, PubMed:27716525). May also play a role in the epigenetic regulation of gene expression by participating in DNA demethylation (PubMed:21496894).

Biological Process

B cell differentiation Source: UniProtKB
Cytidine to uridine editing Source: GO_Central
Defense response to virus Source: GO_Central
DNA cytosine deamination Source: GO_Central
DNA demethylation Source: UniProtKB
mRNA processing Source: UniProtKB-KW
Negative regulation of DNA methylation-dependent heterochromatin assembly Source: UniProtKB
Negative regulation of single stranded viral RNA replication via double stranded DNA intermediate Source: GO_Central
Negative regulation of transposition Source: GO_Central
Regulation of nuclear cell cycle DNA replication Source: UniProtKB
Somatic diversification of immunoglobulins Source: UniProtKB
Somatic hypermutation of immunoglobulin genes

Cellular Location

Cytoplasm; Nucleus. Predominantly cytoplasmic (PubMed:21385873). In the presence of MCM3AP/GANP, relocalizes to the nucleus (By similarity).

Involvement in disease

Immunodeficiency with hyper-IgM 2 (HIGM2): A rare immunodeficiency syndrome characterized by normal or elevated serum IgM levels with absence of IgG, IgA, and IgE. It results in a profound susceptibility to bacterial infections.

PTM

Ser-38 is the major site whereas Thr-27 is the minor site of phosphorylation. Phosphorylation regulates its class-switch recombination activity.2 Publications
Probably monoubiquitinated on several residues by RNF126.

Akbay, B., Germini, D., Bissenbaev, A. K., Musinova, Y. R., Sheval, E. V., Vassetzky, Y., & Dokudovskaya, S. (2021). HIV-1 Tat Activates Akt/mTORC1 Pathway and AICDA Expression by Downregulating Its Transcriptional Inhibitors in B Cells. International journal of molecular sciences, 22(4), 1588.

Mdletshe, N., Nel, A., Shires, K., & Mowla, S. (2020). HIV Nef enhances the expression of oncogenic c-MYC and activation-induced cytidine deaminase in Burkitt lymphoma cells, promoting genomic instability. Infectious Agents and Cancer, 15(1), 1-10.

Hale, L. P. (2020). Deficiency of activation-induced cytidine deaminase in a murine model of ulcerative colitis. Plos one, 15(9), e0239295.

Lio, C. W. J., Shukla, V., Samaniego-Castruita, D., González-Avalos, E., Chakraborty, A., Yue, X., ... & Rao, A. (2019). TET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer. Science immunology, 4(34).

Abdullah, A. M., Elnasri, H. A., Albkrye, A. M., Khaeir, M. A., & Mohmed, H. O. (2019). IN–SILICO ANALYSIS OF NON-SYNONYMOUS SINGLE NUCLEOTIDE POLYMORPHISMS OF ACTIVATION-INDUCED CYTIDINE DEAMINASE (AICDA) GENE. European Journal of Biomedical, 6(11), 30-37.

Kumar, R., & Evans, T. (2019). Activation‐Induced Cytidine Deaminase Regulates Fibroblast Growth Factor/Extracellular Signal‐Regulated Kinases Signaling to Achieve the Naïve Pluripotent State During Reprogramming. Stem Cells, 37(8), 1003-1017.

Burack, R., Li, H., Adlowitz, D. G., Spence, J. M., Leblanc, M. L., Rimsza, L. M., ... & Friedberg, J. W. (2019). Intraclonal Heterogeneity Caused By Activation-Induced Cytidine Deaminase Is Not a Prognostic Biomarker in Untreated Advanced Stage Follicular Lymphoma: An Analysis of SWOG S0016.

Li, Y., Wang, Y., Sun, N., Yang, H., Zhang, Q., Zhang, X., ... & Jia, X. (2019). Activation-induced cytidine deaminase plays crucial role in ovalbumin-induced food allergy and promoted by IL-21. Molecular immunology, 114, 369-377.

Sall, F. B., El Amine, R., Markozashvili, D., Tsfasman, T., Oksenhendler, E., Lipinski, M., ... & Germini, D. (2019). HIV‐1 Tat protein induces aberrant activation of AICDA in human B‐lymphocytes from peripheral blood. Journal of cellular physiology, 234(9), 15678-15685.

El Kadi, N., Wang, L., Davis, A., Korkaya, H., Cooke, A., Vadnala, V., ... & Hassan, K. A. (2018). The EGFR T790M mutation is acquired through AICDA-mediated deamination of 5-methylcytosine following TKI treatment in lung cancer. Cancer research, 78(24), 6728-6735.

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Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
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Proteogenomic
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For research use only. Not intended for any clinical use.

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