HES1 Antibodies

Transcription factor HES-1 (HES1)

Transcriptional repressor of genes that require a bHLH protein for their transcription. May act as a negative regulator of myogenesis by inhibiting the functions of MYOD1 and ASH1.

Binds DNA on N-box themes: 5'-CACNAG-3' with high affinity and on E-box themes: 5'-CANNTG-3' with low affinity (By similarity). May play a part in a functional FA core complex response to DNA cross-link harm, needing the stability and nuclear localization of FA core complex proteins, as well as for FANCD2 monoubiquitination in response to DNA damage.

Gene Information

Human
Gene Name:	HES1
Uniprot:	Q14469
Entrez:	3280

Family

Belongs to:
No superfamily

Alternative Names

BHLHB39; bHLHb39hairy homolog (Drosophila); Class B basic helix-loop-helix protein 39; FLJ20408; Hairy and enhancer of split 1; hairy and enhancer of split 1, (Drosophila); Hairy homolog; Hairy-like protein; HES1; HES-1; hHL; HL; HRY; HRYHHL; transcription factor HES-1

Molecular Weight

Mass (kDA):
29.541 kDA

Genomic Context

Human
Location:	3q29
Sequence:	3; NC_000003.12 (194136148..194138732)

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Idiopathic Hypereosinophilic Syndrome
• Leukemia
• Nervousness
• Carcinoma
• Cell Transformation, Neoplastic
• Pituitary Diseases
• Precursor T-cell Lymphoblastic Leukemia-lymphoma
• Acute Lymphocytic Leukemia
• Malignant Paraganglionic Neoplasm
• Lymphoma
• Malignant Neoplasm Of Breast

• Adenocarcinoma
• Brain Neoplasms
• Dysplasia
• Malignant Neoplasm Of Lung
• Lung Neoplasms
• Tumor Angiogenesis
• Diabetes Mellitus

Interacting Proteins

• SIRT1

Pathways

• Notch Signaling Pathway
• Cell Differentiation
• Cell Proliferation
• Neurogenesis
• Cell Cycle
• Pathogenesis
• Cell Growth
• Regeneration
• Cell Development
• Segmentation
• Localization
• Angiogenesis
• Cell Fate Determination

• Cell Cycle Arrest
• Cell Death
• Somitogenesis
• Lateral Inhibition
• Dedifferentiation
• Rna Interference
• Stem Cell Differentiation

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Acetylation
• Ubiquitination
• Demethylation
• Biotinylation
• Oxidation

• Sumoylation
• Hydroxylation
• Gamma-cleavage
• Ubiquitinylation
• Ribosylation
• Farnesylation
• Glycosylation
• Deacetylation

Research Areas

• Stem Cell Markers

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/HES1

Boster Bio Discovers The Best Uses Of The HES1 Marker

Boster Bio provides high-affinity, validated prima antibodies that have been used by researchers since 1995. The antibodies have been tested for efficacy in immunohistochemistry, Western blotting, and ELISA. Continue reading to learn more about Hes1.

Hes1 is a transcriptional inhibitor

Hes-1, which is one of the most significant Notch effectors in neurogenesis inhibition, is one of the most important. It is a protein ubiquitinated and g-secretase produces it in the body. Hes-1 and Hes-5 are induced by the NICD gene. Neurogenesis is inhibited if these proteins are not present. Hes-1 & Hes-5 operate in a similar signaling pathway. The process is also influenced a SUMO-modified protein PIAS1 or PIAS2.

In cancer, Hes1 plays a crucial role in tumor metastasis. This occurs when cancer cells move from the primary location to another. It demonstrates poor prognosis and increases the risk of death. It is essential to develop therapies that inhibit Hes1. This is why the drug is receiving so much attention. Its clinical advancement is an important aspect in cancer therapy.

The basic domain Lys39 is believed to confer Hes-1 DNA binding activity. SUMOylation could also affect Hes-1's DNA-binding activity. To determine the DNA-binding activity of Hes-1 on the GADD45a promoter, ChIPPCR was used. Lys39 mutation and 3KR mutation decreased the activity of Hes-1 on this promoter.

Hes-1 is also SUMOylated, which decreases the activity of other proteins. Hes-1 SUMOylation is believed to be dependent on PIAS1. The resulting phosphorylation change may alter Hes-1’s DNA binding activity or downstream gene expression. These findings provide a novel treatment method for cancer. Further research is needed to determine the potential role of Hes-1 for cancer therapy.

It is a member the basic helix loop-helix (bHLH).

HES1 is a transcription factor that binds to DNA through a region called the E box. Different bHLH protein families recognize different sequences in the E box, and therefore have different binding affinities. The bHLH molecular motif is made up of two distinct regions. The HLH region is adjacent to the alkaline area. It is associated with binding TFs. The HLH domain is found at the C-terminus of the protein and has two adjacent a-helices.

HES1 not only acts as a transcriptional inhibitor, but also antagonizes many neuronal cell fate regulatory genes, such as Nck and Nflb. As a member of the bHLH family, HES1 is classified as a factor with three conserved domains. It may help maintain neural stem cells.

HES1 is involved with plant development and growth. These proteins belong to the basic helix, loop-helix (bHLH), family of TF genes. Their regulatory role in plant growth and development is well documented. It has also been shown interaction with Stra13 (BMAL1) and Stra13.

The bHLH superfamily includes over 125 proteins in humans, and more than 145 in plants. Our understanding of the bHLH superfamily grew over the past 15 years. Thanks to more genomes being sequenced, we now have a better understanding of its functions. As more genomes are sequenced and structural-genomics collaborations are established, bHLH proteins will continue to be of increasing interest.

It is used in cancer stem cells

The HES1 molecule plays a crucial role in tumor cells. These cells have their own strategies to maintain stemness as well as metastasize and resist chemotherapy. Targeting Hes1 is a possible new therapeutic strategy for treating cancer. In the meantime, clinical development of this molecule should be given significant attention. Here are some potential uses of Hes1 for cancer. Let's have a closer look.

It inhibits the migration, proliferation, and invasion of lung cancer cells. It also inhibits cell proliferation and invasion, which can lead to xenograft growth. In addition, it inhibits the expression of musashi-1 (MSI-1) and snail in human lung cancer cells. However, the role of HES1 in lung cancer cells is not fully understood.

HES1 functions as the mammalian equivalent of Enhancer, Hairy and Hairy. It is vital in controlling many physiological processes such as cell cycle arrest, self-renewal ability, and cell cycle arrest. Cancer stem cells are often abnormal in this pathway. HES1 may be expressed in cancer cells as a sign of an abnormality in these pathways. Researchers may be able identify tumor-specific, cancer stem cells to help them target these cells better.

HES1 could also play a part in the development lung cells. It is also expressed on pancreatic stem cell, intestinal crypt precursor cells, and bone-marrow mesenchymal cells. The Notch–Hes1 pathway regulates development. This pathway is essential to self-renewal of lung CSCs and metastasis.

It is responsible for tumor drug resistance

Boster Bio researchers have discovered a new HES1-related marker that could contribute to tumor drug resistance. The marker is rich in cancer stem cells. Hes1 inhibition leads to decreased stemness in gastric cancer cells. The inhibitor may also have an Anti-Tumor effect. This marker is expressed in many cancers, including those with advanced malignancies. This article describes the mechanism of HES1 and how it contributes in tumor drug resistance.

HES1 expression can be found in many types tumors, such as renal cell carcinoma. The marker helps to prevent tumor drug resistance by aiding the immune system to identify drug-resistant tumours. This is why tumor blood vessels are often inefficient, contributing to high interstitial pressure, hypoxia and acidosis. Multiple drugs that target this marker could be co-first-line agents.

Boster Bio has also identified a new HES1 gene that could be used for targeted therapies. This marker could also be used by doctors to monitor drug resistance. HES1 is a marker that can be used to target cancer cells. This will allow them to target them more effectively with fewer side effects. These agents could also increase tumor specificity. These findings are encouraging and support further research to identify effective cancer drugs. Further research is required to confirm the effectiveness of these therapies. The funding was provided by Jiangsu Province and the National Natural Science Foundation of China.

It may be a therapeutic option to treat cancer

The HES1 gene regulates the immune response. It could be an effective therapeutic target in cancer treatment, as it has demonstrated its therapeutic potential for gastric tumours. It is also known as Diacerin and has 358 amino acid. It interacts with other proteins within the human body, including TFDP2 & E2F1 complicateds.

There are many types of cancers that are associated with the Notch signaling pathway. Inhibitors of the Notch pathway might prevent cancer progression by inhibiting certain molecules. Specific drugs that target tumors may be found by targeting Jagged1 and Dll4 via Notch signaling. Many types of cancer, including head and neck and gastric, are caused by the HES1 gene.

Nearly a century has passed since the discovery of Notch signaling. Numerous studies have also shown its role oncogenic processes. In gastric cancer, a high-expression of Notch components is associated with an increased risk for cancer. Numerous anti-cancer drugs have been linked to Notch signaling. It is not yet clear if Notch targeting will be an effective treatment for cancer.

A new marker, which recognizes tumor-associated macrophages, is a novel approach to treating cancer through immunotherapy. Despite the potential benefits, there are potential side effects. TAMs are complex to reprogramme in tumors. Patients with cancer may also experience a refractory immune response.