YAP1 Antibodies

Transcriptional coactivator YAP1 (YAP1)

Transcriptional regulator which can act both as a coactivator and a corepressor and is the crucial downstream regulatory target in the Hippo signaling pathway that plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis (PubMed:17974916, PubMed:18280240, PubMed:18579750, PubMed:21364637). The core of this pathway is made up of a kinase cascade wherein STK3/MST2 and STK4/MST1, in complex with its own regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its own regulatory protein MOB1, which then phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ (PubMed:18158288).

Plays a key role in tissue tension and 3D tissue shape by regulating cortical actomyosin network formation. Acts via ARHGAP18, a Rho GTPase activating protein that inhibits F-actin polymerization (PubMed:25778702).

Gene Information

Human
Gene Name:	YAP1
Uniprot:	P46937
Entrez:	10413

Family

Belongs to:
YAP1 family

Alternative Names

65 kDa Yes-associated protein; YAP; YAP1; YAP2; YAP65; YAP65yes-associated protein 2; Yes-associated protein 1; Yes-associated protein 1, 65kDa; yes-associated protein beta; yes-associated protein delta; YKI; Yorkie Homolog

Molecular Weight

Mass (kDA):
54.462 kDA

Genomic Context

Human
Location:	11q22.1
Sequence:	11; NC_000011.10 (102109957..102233424)

Tissue Specificity

Increased expression seen in some liver and prostate cancers. Isoforms lacking the transactivation domain found in striatal neurons of patients with Huntington disease (at protein level).

Subcellular Localizations

Cytoplasm. Nucleus. Both phosphorylation and cell density can regulate its subcellular localization. Phosphorylation sequesters it in the cytoplasm by inhibiting its translocation into the nucleus. At low density, predominantly nuclear and is translocated to the cytoplasm at high density (PubMed:18158288, PubMed:20048001). PTPN14 induces translocation from the nucleus to the cytoplasm (PubMed:22525271).

Diseases

• Neoplasms
• Malignant Neoplasms
• Cell Transformation, Neoplastic
• Carcinoma
• Malignant Neoplasm Of Breast
• Physiological Stress
• Malignant Squamous Cell Neoplasm
• Neoplasm Metastasis
• Adenocarcinoma
• Cell Invasion
• Tissue Adhesions
• Hyperplasia

• Liver Neoplasms
• Lung Neoplasms
• Liver Carcinoma
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Lung
• Malignant Neoplasm Of Pancreas
• Malignant Neoplasm Of Stomach

Interacting Proteins

• AXIN1
• Axin1
• CTNNB1
• DDX17
• ERBB4

• LATS1
• MAP2K1
• PRKAA1
• Prkaa1
• PRRG2

• PTCH1
• PTPN14
• RAB11A
• RUNX1
• SCRIB

• SMAD1
• SMAD7
• SOCS6
• TBX5
• TEAD1

• TEAD2
• TEAD4
• TP73
• WBP1
• Wbp1

• WBP2
• YWHAB
• YWHAE
• YWHAZ

Pathways

• Localization
• Response To Oxidative Stress
• Cell Proliferation
• Drug Resistance
• Cell Growth
• Transport
• Hypersensitivity
• Cell Cycle
• Cell Death
• Nuclear Export
• Translation
• Pathogenesis
• Virulence

• Dna Repair
• Glycolysis
• Cell Division
• Response To Hydrogen Peroxide
• Protein Oxidation
• Proteolysis
• Contact Inhibition

PTMs

• Phosphorylation
• Oxidation
• Reduction
• Cleavage
• Ubiquitination
• Methylation

• Sumoylation
• Dephosphorylation
• Carboxylation
• Biotinylation
• Deacetylation
• Acetylation

Research Areas

• Breast Cancer
• Cancer
• Chromatin Research
• Core ESC-Like Genes
• Signal Transduction

• Stem Cell Markers
• Transcription Factors and Regulators
• Tyrosine Kinases

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/YAP1

Best Uses Of The YAP1 Marker

YAP1 is a transcriptional coactivator and interacts directly with HIF-1a. It is a key regulator of the stability of HIF-1a and may act as an oncogene in certain cases. This marker can be used in your research to determine whether it is involved with the proliferation of cancer cells. There are a lot of questions this marker can answer, and Boster Bio's optimization guides can help you find the best results possible.

YAP1 is a transcriptional co-activator

While the function of YAP1 remains elusive, it is known that it regulates several genes. It interacts with Birc2 in the same way as TEAD and has been implicated in regulating CTGF and amphiregulin. It also regulates Hoxa1 and Hoxc13, which prevent the transcription of these genes. It is unclear how YAP1 regulates transcription, however it is possible that the gene acts as a transcriptional coactivator.

In an RNAi screen, researchers identified YAP as a gene required for anchorage-independent growth and survival of b-catenin-active cancer cells. Interestingly, the inhibition of TAZ did not affect the cell proliferation. In addition, they found that YAP was in synergy with TBX5 under the YES1 Kinase to increase the expression of BIRC5 and BCL2L1. However, YAP and TAZ are not yet known to directly regulate Wnt signaling pathways, and the interaction between these two pathways remains unclear.

The role of YAP in stem cell behavior has not been thoroughly understood, however, it is believed that it is required to promote self-renewal and the suppression of differentiation in ES cells. Furthermore, the the overexpression of YAP leads to an expanded pool of progenitors that are not differentiated in the mouse crypt which suggests that YAP plays a role in regulating neural progenitor cells numbers. Yorkie, a gene associated with YAP also regulates the number of stem cells in the Drosophila crypt.

The development of solid tumors is influenced by the Hippo signaling pathway. YAP1 as well as TAZ are downstream effects of this pathway. Furthermore, dysregulation of the Hippo pathway could serve as a marker of prognosis for cancer progression and could be a target for targeted therapies. Furthermore, since YAP is involved in cancer cell proliferation and apoptosis, it's an important gene in many human diseases.

YAP1 plays a role in the development and growth of tumors. It also aids in the development of EMT, stem-cell-associated genes, and other related processes. It can also cause resistance to chemotherapy and the formation of metastasis. Understanding the significance of YAP1 and colon cancer requires more studies, as well as more high-quality samples from patients. So far, these genes are associated with the progression of the disease and will remain a source of useful information.

It is directly connected to HIF-1a.

Cardiogenesis is a multifaceted process that involves cell differentiation. Different types of cells play a role in the heart's development, including adipocytes and myocardial fibroblasts. The genes YAP1/TAZ play a key role in this process. However, when these two genes are shut down, embryos fail to survive beyond E15.5. However, overexpression of these genes stops them from becoming cardiac fibroblasts. Normal development and growth of the heart is dependent on YAP1/TAZ activities.

YAP1 has a significant role in stem cell expansion and dedifferentiation. In addition to its role in stem cell growth, it is vital for adult CM renewal after injury. The presence of an E3 Ubiquitin Protein Complex (SCFbTRCP) regulates activation of this gene.

YAP1 inhibits the DNA-damage chain of events, which includes the genes ATR and ATM. These genes trigger apoptosis if they detect excessive DNA damage. Additionally, YAP1 promotes mitochondrial homeostasis. This stimulates fusion and decreases the Apoptosis. It is not clear what the reason is YAP1 regulates the cardiac development in endocardial tissues.

In the field of cardiac biology, the Hippo-YAP1/TAZ pathway is used. The YAP1 receptor is phosphorylated in the essential Hippo pathway components and then degraded in the cell cytoplasm. The active YAP1/TAZ migrate to the nucleusand there they join with transcriptional partners. These proteins regulate cardiac output by their activities. The two proteins are controlled by a variety of upstream pathways as well as cell-cell junctions.

It regulates the stability of HIF-1a.

In a recent study researchers found that YAP1 overexpression was associated with increased levels of HIF-1a in human colorectal cancer tissues under hypoxia. It is believed that YAP1 plays an important role in controlling cell glycolysis through HIF-1a. In addition, YAP1 is thought to regulate the stability of HIF-1a within the nucleus. These results suggest that YAP could be a potential therapeutic target for HCC.

When Hippo signaling is off The YAP1 gene is activated and transferred to the nucleus. YAP1 is not a DNA-binding domains and instead interacts with transcriptional partner proteins such as TEADs and the Smad family, and p63/p73. The specific biological output of YAP1 is determined by its binding site.

The NF2 CKO heart is protected from IR injury through an increase in YAP1 activity. This may be due to its ability to regulate autophagy, and consequently reduce IR damage. Therefore, MST1 could act as a negative regulator of cardiac protection by mechanisms involving the Hippo pathway. Furthermore, the Hippo pathway could be involved in the heart's anti-survival function.

Normal recovery and development of the cardiac muscle are dependent on the YAP1/TAZ pathway. The rate of cardiogenesis is a factor that determines the activity of the YAP1/TAZ pathway. The YAP1/TAZ activities should be adjusted in accordance with the speed of cardiogenesis. These interactions are vital for cardiogenesis. There is also an ongoing study to determine whether YAP1 and HIF-1a play a role in the tyrosine-phosphorylation of the TEAD protein.

HIF-1a and PHD2 are also linked through the persulfidation the zinc finger motif of PHD1. CBS assists in the persulfidation of PHD2 in its cysteine residues inside its zinc finger. The VHL eventually recognizes the HIF-1a complex and it is degraded through proteasomal degradation. When hypoxia is present, both PHD1 and CBS activity are diminished. Both proteins are downregulated, which decreases H2S levels.

In hypoxia, the expression of GPRC5Asi1R must be present to rescue hypoxia-induced symptoms. Hypoxia triggers GPRC5A to activate YAP through Hippo pathway activator YAP. Hypoxia promotes apoptosis of hypoxic cancer cells via suppression of BCL-XL activation. YAP could be a novel therapeutic target.

In some cases it functions as an oncogene

It is one of a variety of transcription factors that play a role in a myriad of cells. The YAP1 gene is involved in recruitment of numerous downstream target genes. These targets are connected to cell proliferation, migration and angiogenesis. In some instances, YAP1 acts as an oncogene through the upregulation of these genes. The precise mechanisms that YAP1 causes cell death are being investigated.

Activation of YAP1 in cancer is a consequence of malfunctions in the Hippo pathway and amplification of the 11q22 genomic locus. Although the role of YAP1 is still a matter of debate research has shown that YAP1 expression in breast cancer is higher in luminal and invasive than normal breast tissue. Additionally, YAP1 can regulate cell proliferation and invasion.

The YAP/Hippo pathway is frequently disrupted in cancerous cells in humans. The absence of coordination in these pathways causes an increase in tumor size and growth in the tissues, which are common features of many diseases. Both YAP and the signaling pathways p53 are vital for normal development of the body and the interaction between the two could trigger both oncogenic and tumor suppressor effects, depending on their respective levels.

YAP also regulates Stearoyl-CoA-desaturase-1 (SCD1). YAP is overexpressed in lung cancer stem cells boosts the amount of NMU. It also enhances cell motility and tumor invasion. It also inhibits cell cycle and the process of apoptosis. It is possible that downregulation of the LATS1 gene leads to a number of different malignancies, like lung cancer.

YAP1 is present in various cancers. It alters the metabolism of cells by altering the transcription of pro-apoptotic genes when it is in response to DNA damage signals. It has been linked to Alzheimer's disease, a form dementia. The expression of p53 was found to be a key factor in the function of YAP for brain disorders. Its regulation is vital in curing and preventing these diseases.

There are many other factors that can trigger tumor growth in people with YAP1 gene expression. These include the stage of tumor development, genetics and age. It has also been demonstrated that YAP1 expression is related to OS in ccRCC. It could be a reliable predictor of survival in ccRCC.