Mouse Anti-IGHG1 Recombinant Antibody (ICO-97) (CBMAB-I0197-YY)

Name: Mouse Anti-IGHG1 Recombinant Antibody (ICO-97)
SKU: CBMAB-I0197-YY
Rating: 5 (1 reviews)

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Datasheet

SDS

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

Basic Information

Host Animal

Mouse

Clone

ICO-97

Application

FC, ELISA

Specificity

Human

Antibody Isotype

IgG1

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

Liquid

Buffer

50 mM Na3PO4, pH 7.5, 100 mM KCl, 150mM NaCl, 5% Glycerol, 0.2% BSA, 5% Glycerol

Concentration

1.0 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

Immunoglobulin heavy constant gamma 1

Introduction

IGHG1 (Immunoglobulin Heavy Constant Gamma 1 (G1m Marker)) is a Protein Coding gene. Diseases associated with IGHG1 include Leukemia, Chronic Lymphocytic and Heavy Chain Deposition Disease. Among its related pathways are Creation of C4 and C2 activators and Role of phospholipids in phagocytosis.

Entrez Gene ID

3500

UniProt ID

P01857

Alternative Names

Immunoglobulin Heavy Constant Gamma 1 (G1m Marker)

Function

Constant region of immunoglobulin heavy chains. Immunoglobulins, also known as antibodies, are membrane-bound or secreted glycoproteins produced by B lymphocytes. In the recognition phase of humoral immunity, the membrane-bound immunoglobulins serve as receptors which, upon binding of a specific antigen, trigger the clonal expansion and differentiation of B lymphocytes into immunoglobulins-secreting plasma cells. Secreted immunoglobulins mediate the effector phase of humoral immunity, which results in the elimination of bound antigens (PubMed:22158414, PubMed:20176268).

The antigen binding site is formed by the variable domain of one heavy chain, together with that of its associated light chain. Thus, each immunoglobulin has two antigen binding sites with remarkable affinity for a particular antigen. The variable domains are assembled by a process called V-(D)-J rearrangement and can then be subjected to somatic hypermutations which, after exposure to antigen and selection, allow affinity maturation for a particular antigen (PubMed:17576170, PubMed:20176268).

Mediates IgG effector functions on monocytes triggering ADCC of virus-infected cells.

Biological Process

B cell receptor signaling pathway Source: GO_Central
Complement activation, classical pathway Source: GO_Central
Defense response to bacterium Source: GO_Central
Innate immune response Source: GO_Central
Phagocytosis, engulfment Source: GO_Central
Phagocytosis, recognition Source: GO_Central
Positive regulation of B cell activation Source: GO_Central

Cellular Location

Secreted; Cell membrane

Involvement in disease

Multiple myeloma (MM):
The disease is caused by variants affecting the gene represented in this entry. A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4. A malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia.

Jin, Y., Qiu, L., Bao, W., Lu, M., Cao, F., Ni, H., & Zhao, B. (2023). High expression of IGHG1 promotes breast cancer malignant development by activating the AKT pathway. Cell Cycle, 22(6), 718-731.

Tian, Y., Han, W., Fu, L., Lv, K., & Zhou, X. (2023). Silencing of IGHG1 reverses the resistance of pancreatic cancer to multidrug chemotherapy by modulating autophagy. Environmental Toxicology.

Li, Y., Yun, X., Li, J., & Bai, M. (2023). CSTF2T up-regulates IGHG1 by binding to ZEB1 to promote melanoma cell proliferation, migration, and invasion. Tissue and Cell, 81, 102029.

Zhang, Y., Fang, X., & Sun, Y. (2023). IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling. Biomolecules and Biomedicine.

Li, Y., Wang, P., Ye, D., Bai, X., Zeng, X., Zhao, Q., & Zhang, Z. (2021). IGHG1 induces EMT in gastric cancer cells by regulating TGF-β/SMAD3 signaling pathway. Journal of Cancer, 12(12), 3458.

Li, X., Chen, W., Yang, C., Huang, Y., Jia, J., Xu, R., ... & Xie, L. (2021). IGHG1 upregulation promoted gastric cancer malignancy via AKT/GSK-3β/β-Catenin pathway. Cancer Cell International, 21, 1-12.

Yang, G., Li, G., Du, X., Zhou, W., Zou, X., Liu, Y., ... & Li, Z. (2021). Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis. Open Life Sciences, 16(1), 930-936.

Chu, J., Li, Y., Deng, Z., Zhang, Z., Xie, Q., Zhang, H., ... & Pan, B. (2019). IGHG1 regulates prostate cancer growth via the MEK/ERK/c-Myc pathway. BioMed Research International, 2019.

Qian, J., Ji, F., Ye, X., Cheng, H., Ma, R., Chang, X., ... & Cui, H. (2018). IGHG1 promotes motility likely through epithelial-mesenchymal transition in ovarian cancer. Chinese Journal of Cancer Research, 30(2), 282.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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