MYCL Antibodies

Background

The MYCL gene, as a member of the MYC proto-oncogene family, encodes a transcription factor with a helical-ring-helical structure. This protein regulates the expression of genes related to cell cycle progression, proliferation and differentiation, and metabolism by forming a heterodimer with the MAX protein and binding to the E-box sequence. In malignant tumors such as lung cancer and neuroblastoma, MYCL is often abnormally highly expressed due to gene amplification or transcriptional activation, driving abnormal proliferation of tumor cells. Researchers first identified this gene in a mouse lung cancer model in 1983, and its human homolog L-MYC was discovered the following year. Due to the relative instability of the MYCL protein structure and its interaction with multiple signaling pathways, it has become an important model system for studying targeted cancer therapy and transcriptional regulation mechanisms.

Structure Function Application Advantage Our Products

Structure of MYCL

The L-MYC protein encoded by the MYCL gene is a nuclear transcription factor with a molecular weight of approximately 38-40 kDa, and its precise molecular weight varies slightly due to post-translational modifications and species differences. This protein belongs to the basic helical-ring-helix (bHLH) family, and its structure is mainly mediated by the conserved bHLH domain for protein dimerization and DNA binding. L-MYC binds to its dimerization partner MAX protein, recognizes the E-box cis-element, and thereby regulates the transcription of downstream target genes, affecting the cell cycle, proliferation and metabolic processes. Compared with c-MYC, L-MYC has structural differences in the transcriptional activation domain, and its carcinogenic activity is relatively weak. However, amplification or overexpression is still common in small cell lung cancer and neuroblastoma.

Fig. 1:Schematic representation of WT c-MYC and MYCL protein. Fig. 1 Schematic representation of WT c-MYC and MYCL protein.¹

Key structural properties of MYCL:

Alkaline helical ring-helical (bHLH) and leucine zipper (ZIP) domains
Conserved bHLH-ZIP mediates dimerization with MAX protein and DNA binding
The short transcriptional activation domain (TAD) is less active than c-MYC

Functions of MYCL

The main function of the MYCL gene is to act as a transcription factor to regulate cell proliferation and differentiation. However, it is also widely involved in various pathological processes, including tumorigenesis and metabolic reprogramming.

Function	Description
Transcriptional activation	Combined with MAX proteins to form dimers, E - box series, activation, proliferation and cell cycle related gene transcription.
Tumorigenesis driver	In small cell lung cancer and neuroblastoma abnormally high expression, promote the development of cell proliferation and malignant tumor.
Metabolic regulation	Affects cancer-related metabolic pathways such as glycolysis and glutamine metabolism, supporting the energy and biosynthetic needs of tumor cells.
Regulation of the cell cycle process	Up-regulate the expression of key cyclins such as Cyclin D1 and CDK4, and accelerate the G1/S phase transition.
Differentiation inhibition	Inhibit the terminal differentiation program in multiple cell types to maintain the cells in an undifferentiated proliferative state.

The dimer formed by MYCL and MAX protein preferentially recognizes the CACGTG sequence. Its transcriptional activity highly depends on the upstream and downstream regulatory sequences and histone modification status. Compared with c-MYC, it shows a narrower target gene spectrum and weaker carcinogenic potential.

Applications of MYCL and MYCL Antibody in Literature

1. Akifuji, Chiaki, et al. "MYCL promotes iPSC-like colony formation via MYC Box 0 and 2 domains." Scientific Reports 11.1 (2021): 24254. https://doi.org/10.1038/s41598-021-03260-5

This study explores the molecular mechanism by which MYCL is more efficient than c-MYC in reprogramming. It was found that the MB0 and MB2 domains of MYCL respectively regulate cell adhesion and RNA processing, thereby enhancing the induction efficiency of hiPSC.

2. Kato, Fuyumi, et al. "MYCL is a target of a BET bromodomain inhibitor, JQ1, on growth suppression efficacy in small cell lung cancer cells." Oncotarget 7.47 (2016): 77378. https://doi.org/10.18632/oncotarget.12671

This study explored the effect of BET inhibitor JQ1 on small cell lung cancer (SCLC) with MYCL expression/amplification. It was found that JQ1 can generally inhibit the growth of SCLC cells and down-regulate genes such as MYCL, but its sensitivity does not depend on the level of MYCL, but is related to the expression and inhibition degree of CDK6.

3. Cheng, gwei, et al. "Merkel cell polyomavirus recruits MYCL to the EP400 complex to promote oncogenesis." PLoS pathogens 13.10 (2017): e1006668. https://doi.org/10.1371/journal.ppat.1006668

This study reveals that the ST antigen in Merkel cell carcinoma binds to MYCL and is recruited into the EP400 chromatin remodeling complex, jointly activating the expression of specific genes, promoting malignant transformation of cells and maintaining cell activity.

4. Fong, K. M., et al. "MYCL genotypes and loss of heterozygosity in non-small-cell lung cancer." British journal of cancer 74.12 (1996): 1975-1978. https://doi.org/10.1038/bjc.1996.662

This study found that the MYCL genotype was not related to tumor progression or prognosis in 108 cases of non-small cell lung cancer (NSCLC), but the heterozygous deletion (LOH) at the 1p32 locus of this chromosome was significantly associated with lymph node metastasis and advanced TNM stage, suggesting that there may be tumor suppressor genes related to tumor progression in the vicinity.

5. Liu, Zhihui, et al. "Targeting MYCN in pediatric and adult cancers." Frontiers in oncology 10 (2021): 623679. https://doi.org/10.3389/fonc.2020.623679

This study reviews the abnormal regulation and targeting strategies of MYC family oncogenes (including MYCL) in tumors, focuses on exploring the structural and functional similarities, expression differences between MYCN and c-MYC, as well as their roles in development and tumors, and summarizes the research progress of MyCN-targeted treatment.

Creative Biolabs: MYCL Antibodies for Research

Creative Biolabs specializes in the production of high-quality MYCL antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

Custom MYCL Antibody Development: Tailor-made solutions to meet specific research requirements.
Bulk Production: Large-scale antibody manufacturing for industry partners.
Technical Support: Expert consultation for protocol optimization and troubleshooting.
Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our MYCL antibodies, custom preparations, or technical support, contact us at email.

Reference

Akifuji, Chiaki, et al. "MYCL promotes iPSC-like colony formation via MYC Box 0 and 2 domains." Scientific Reports 11.1 (2021): 24254. https://doi.org/10.1038/s41598-021-03260-5