Myb-related protein B Antibodies

Myb-related protein B (MYBL2)

Transcription factor involved in the regulation of cell survival, proliferation, and differentiation. Transactivates the expression of the CLU gene.

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Gene Information

Human
Gene Name:	MYBL2
Uniprot:	P10244
Entrez:	4605

Family

Belongs to:
No superfamily

Alternative Names

B-MYB; BMYBMGC15600; Myb-like protein 2; myb-related protein B; v-myb avian myeloblastosis viral oncogene homolog-like 2; v-myb myeloblastosis viral oncogene homolog (avian)-like 2

Molecular Weight

Mass (kDA):
78.764 kDA

Genomic Context

Human
Location:	20q13.12
Sequence:	20; NC_000020.11 (43667019..43716496)

Subcellular Localizations

Nucleus.

Diseases

• Neoplasms
• Malignant Neoplasms
• Retinoblastoma
• Carcinoma
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Neuroblastoma
• Cell Transformation, Neoplastic
• Leukemia
• Adenocarcinoma
• Neoplasm Metastasis
• Malignant Paraganglionic Neoplasm
• Carcinogenesis

• Osteosarcoma
• Liver Carcinoma
• Prostatic Neoplasms
• Colorectal Cancer
• Cytogenetic Abnormality
• Malignant Neoplasm Of Prostate
• Myeloid Leukemia

Interacting Proteins

• LIN54
• LIN9

Pathways

• Cell Cycle
• S Phase
• Cell Proliferation
• Localization
• Pathogenesis
• G1 Phase
• Cell Death
• Cell Growth
• Senescence
• Spermatogenesis
• Cellular Senescence
• Mitosis
• Cell Maturation

• Dna Amplification
• Cell Cycle Arrest
• Regulation Of Cell Cycle
• Oncogenesis
• Dna Replication
• Programmed Cell Death
• Aging

PTMs

• Phosphorylation
• Acetylation
• Dephosphorylation
• Reduction

• Cleavage
• Oxidation
• Methylation
• Ubiquitination

Research Areas

• Apoptosis
• Cancer
• Core ESC-Like Genes
• Stem Cell Markers

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MYBL2

Boster Bio - Best Uses Of The MYBL2 Marker

The MYBL2 marker plays a significant role in the advancement of cell cycle progression. It is also a key regulator of cell survival, and is a factor in the malignant phenotype that is associated with cancer cells. The boster bio MYBL2 is applicable to scientists around the world. Find out more about the MYBL2 marker. Let's start by going over the boster bioassay process.

MYBL2 is one of the transcription elements.

The mRNA expression data for MYBL2 were obtained from the Cancer Genome Atlas database (TCGA). In July 2019, researchers analyzed 611 gene expression profiles of MYBL2 from CCRCCs. Researchers discovered that MYBL2 expression was significantly higher in ccRCc tissues than in normal tissues. MYBL2 expression was also associated with the increased expression of the apolipoprotein-mRNA editing catalytic unit of the enzyme 3F.

Researchers found that MYBL2 was significantly increased in ccRCC. This type of cancer is commonly characterized by high-grade dysplasia and poor prognosis. Utilizing gene set enrichment analysis they discovered that MYBL2 is a possible biomarker and therapeutic target. However, further studies are required to understand the precise role of MYBL2 in CCRC.

MYBL2 is extremely expressed in ccRCC tissues and these cells have a tendency to develop metastatic disease. This could be due to of increased expression of the gene, or simply because MYBL2 has a higher degree of expression in tumors. Additionally, MYBL2 is significantly upregulated in the tissues of patients with CCRC. The study also found that MYBL2 is a transcription factor.

MYBL2 is found in both ovarian and breast cancer tissues and its expression was associated with increased proliferative capacity. It isn't clear what MYBL2 can promote proliferation of cells. It is a binder to the A3B promoter in breast cancer cells. This triggers transactivation. It was also discovered that MYBL2 is the only factor that directly controls CENPA expression. These findings suggest that MYBL2 could be a target therapy for ovarian carcinoma.

Numerous studies have been conducted that have linked MYBL2 to a range of malignant or inflammatory conditions. Drugs that target JAK/STAT could be beneficial in the treatment of cancer and immune-mediated diseases. MYBL2 downregulation causes cell cycle arrest in the G2/M phase, and downregulation activates the p53-p21-DREAM-CDE/CHR pathway. MYBL2 could thus be a promising therapeutic target in the treatment of cancer.

MiR-29 and miR-30 are microRNAs targeting the 3'UTR on the B-Myb oncogene. This suggests that the two miRs may regulate the expression of MYBL2 in the process of replicative senescence. The function of MYBL2 for tumor suppression is not fully understood. The evidence is not in support of the idea that miR-30 and miR-29 are the only two genes that directly control the MYBL2 genes.

It is a major regulator of cell cycle progression

MYBL2 is one of the many oncogenes linked to poor prognosis as well as increased cell proliferative capacity. The mechanism through which B-Myb influences the cell cycle isn't fully understood however it has been proven to interact with the MuvB core complex, which is responsible for the transcription of mitotic genes. The B-Myb gene also interacts with the Rb-like protein, p130. This results in formation the DREAM complex which mediates global repression of cell cycle genes in G0/G1.

The growth of cells has been linked with the overexpression of MYBL2. Overexpression of this protein in cancer cells has been linked with aggressive disease progression. Overexpression of MYBL2 is associated with a poor prognosis. Additionally, MYBL2 acts as a potential therapeutic target. It binds to the A3B promoter and activates the gene, which regulates cell cycle progression.

In NSCLC cells, MYBL2 is upregulated leading to an imbalanced cell cycle regulation. This causes the progression of liver cancer by increasing the number of leukemic blasts. It also regulates cell growth and apoptosis. MYBL2 activity is controlled by the transcription factor CCNA1. This protein plays an important role in the S phase of cancer cells"cell cycle.

B-Myb is a transactivating protein. It is a transcriptional element and is involved in interacting with cyclin B-Cdk2 and cyclin regulate the progression of cell cycles. It isn't certain how it regulates the cell cycle. A deeper analysis of this protein might help us to understand the role it plays in the cell cycle. The next step is to investigate whether B-Myb is able to prevent DNA damage.

Low OS in primary hepatocellular carcinoma is associated with high MYBL2 levels. Additionally, high levels of MYBL2 in cancer cells could be a therapeutic target for treating cancer. Ginkgetin is able to regulate b-Myb using miR-34a. Ginkgetin can be used as a chemotherapy agent to treat colorectal cancer.

In the transition from one phase to the next, a set of genes known as M/G1 (M/G1) is expressed. This group includes genes involved in membranes as well as the actin cytoskeleton. It also involves genes implicated in cell-cell interactions. If MYBL2 is a central control of cell cycle progression the mitotic shake-off stage of the cell cycle will be reinstated.

It is a key regulator of cell survival

This gene regulates the cell cycle and plays a vital role in proliferating cells. While it is not detectable during the G0 phase the expression of this gene is elevated during the G1/S transition phase of the cell cycle. MYBL2 is involved in the proliferation of cells and carcinogenesis. Its expression in cancer cells has been linked to poor outcomes in cancer patients. Therefore, further research into MYBL2 is required.

This study explored the relationship of MYBL2 expression with OS in primary Hepatocellular Carcinoma. We also explored the potential role of B-Myb TRA. Utilizing cBioportal we looked at the expression of genes that were linked with MYBL2 Bioinformatics analysis was used to identify the genes that are involved in B-Myb TRA and TP53. Also, statistical tests were used to determine the importance of MYBL2 or TP53 expression in cancer.

Knockdown of MYBL2 is a significant inhibitor of the growth of 22RV1 cells in the absence of androgens. MYBL2 may be involved in metastatic CRCPC growth. YAP is a similar protein to MYBL2 also collaborates in conjunction with MYBL2 in promoting the expression of mitosis-related genes. This supports the liver cancer and lung cell growth. Further research is needed to determine if there is cross-talk between MYBL2 YAP.

The overexpression of MYBL2 oncogene results in increased cell proliferation, and a poor prognosis in cancer. Although the exact mechanism of B.Myb's actions is still to be identified however, it is believed to interact with DREAM complex to alter the expression of cell cycle genes. It is in contact with the Rb-like protein , p130 that represses the majority of cell cycle genes when it is in the phase of quiescence. The MuvB core is recruited by MYBL2 to coordinate late cell cycle gene expression G2/M genes.

The rabbit antibody against MYBL2 was used in the study. It also included anti-YAP proteins derived from rats and mouse. Other antibodies used to study MYBL2 included anti-RAGAP1, Anti-TAZ and anti-LATS1 antibody. The results of this study indicate that a high mutation rate of these proteins is linked with NSCLC. This is why MYBL2 is a key regulator of tumorigenesis.

It is a contributor to the malignant phenotype cancer cells.

The cellular membrane is crucial for many purposes including social interaction and adhesion to cells and structures. It also permits access to nutrients and recognition by the immune system. Malignant cells exhibit abnormal properties that include the absence of the growth inhibition dependent on density as well as a diminished ability to adhere, reduced adhesiveness and anchorage dependence, and increased invasiveness across normal barriers to tissue. Malignant cells also alter the biochemical properties of their surfaces.