bladder cancer

CCDC112 Protein, Human, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 61.0 kDa and the accession number is Q8NEF3.

Ube2T is the E2 ubiquitin-conjugating enzyme of the Fanconi anemia DNA repair pathway and it is overexpressed in several cancers, representing an attractive target for the development of inhibitors. Notably, UBE2T locates at 1q32.1, and the gain of 1q is frequently observed in a variety of cancers. For instance, UBE2T serves an important role in the growth of bladder cancer cells, and may be considered as a potential biomarker and therapeutic target for bladder cancer.

Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) belongs to the immunoglobulin superfamily, which has the homology to both the immunoglobulin V domain and MHC class II antigen β-chain. EMMPRIN is a transmembrane glycoprotein with different forms, resulting from different modes of glycosylation and N-terminal sequence variants. EMMPRIN can be expressed in breast cancer, oral squamous cell carcinoma, glioma, lymphoma, lung, bladder, and melanoma carcinomas cells. EMMPRIN promotes invasion, metastasis, growth, and survival of malignants cells, serves as a receptor for extracellular cyclophilinthe, may play a role in signal transduction.

CD164 was found to play a role in many malignant diseases. CD164 was associated with clinical and pathological features of patients. High level of CD164 was related to the distant metastasis and vascular invasion of bladder cancer patients.CD164 was associated with the poor clinical outcomes of BC patients. Silencing of CD164 could inhibit the progression of tumors in vivo and in vitro, which may become an effective target in the treatment of bladder cancer. CD164 Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 41.4 kDa and the accession number is Q9R0L9.

MTSS1 (Metastasis suppressor 1), also known as Missing in metastasis (MIM), is a tissue-specific regulator of plasma membrane dynamics. MTSS1 is well described for its function as a metastasis suppressor gene and is expressed in a variety of tissues. MTSS1 might be involved in shaping neuronal membranes in vivo. MTSS1 deforms phosphoinositide-rich membranes through its I-BAR domain and interacts with actin monomers through its WH2 domain. MTSS1/MIM was first identified as a metastasis suppressor missing in metastatic bladder carcinoma cell lines. MTSS1 is a prognostic indicator of disease-free survival in breast cancer patients and demonstrates the ability to play a role in governing the metastatic nature of breast cancer cells. MTSS1 may serve as a useful biomarker for the prediction of the outcome of gastric cancer. The down-regulation of MTSS1 that may be caused by DNA methylation was also observed in many other types of cancer. Recent work proposed that MIM also potentiates Sonic hedgehog (Shh)-induced gene expression. MTSS1 is a multiple functional molecular and has an important role in development, carcinogenesis, and metastasis.

The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis. UNC5A Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 58.3 kDa and the accession number is Q6ZN44-1.

OGN (Osteoglycin) is a Protein Coding gene. This gene encodes a member of the small leucine-rich proteoglycan (SLRP) family of proteins. It belongs to the small leucine-rich proteoglycan (SLRP) family. The encoded protein induces ectopic bone formation in conjunction with transforming growth factor-beta and may regulate osteoblast differentiation. OGN is broadly expressed in the gall bladder, endometrium, and other tissues. OGN reduced Zeb-1 expression via EGFR/Akt leading to inhibition of epithelial-mesenchymal transition. In vitro and in vivo, the OGN expression was demonstrated to reduce cell proliferation, inhibit invasion of colon cancer cells then impede cancer progression. Diseases associated with OGN include Inhibited Male Orgasm and Cornea Plana.

PCDH7, a member of protocadherins family, functions as tumor suppressor in several human cancers. The human PCDH7 gene is localized in chromosome 4p15, which is often inactivated in human cancers, including bladder cancer. The low PCDH7 expression is a potential prognostic biomarker for primary non-muscle invasive bladder cancer (NMIBC). PCDH7 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in Baculovirus insect cells with His and Avi tag. The predicted molecular weight is 95.25 kDa and the accession number is NP_002580.2.

NOTCH2 (Notch Receptor 2) is a Protein Coding gene. This gene encodes a member of the Notch family. Members of this Type 1 transmembrane protein family share structural characteristics and play a role in a variety of developmental processes by controlling cell fate decisions. Hajdu Cheney Syndrome (HCS) is a rare disease associated with mutations of NOTCH2 that lead to the translation of a truncated, presumably stable, NOTCH2 protein. NOTCH2 is down-regulated in colon cancer, and reduced expression is associated with a less differentiated, more aggressive phenotype, and reduced overall survival. NOTCH2 has also been shown to have pro-apoptotic and growth-suppressive effects in thyroid carcinoma, and carcinoid tumors. NOTCH2 acts as an oncogene that promotes bladder cancer growth and metastasis through EMT, cell-cycle progression, and maintenance of stemness.

The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis. UNC5A Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 32.7 kDa and the accession number is Q6ZN44-1.

The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Rat, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 65.7 kDa and the accession number is O08722.

PCDH7, a member of protocadherins family, functions as tumor suppressor in several human cancers. The human PCDH7 gene is localized in chromosome 4p15, which is often inactivated in human cancers, including bladder cancer. The low PCDH7 expression is a potential prognostic biomarker for primary non-muscle invasive bladder cancer (NMIBC). PCDH7 Protein, Human, Recombinant (His) is expressed in Baculovirus insect cells with His tag. The predicted molecular weight is 94 kDa and the accession number is O60245-1.

Annexin A10 (ANXA10) contains four Annexin repeats and is a member of the Annexin family. Members of this calcium-dependent phospholipid-binding protein family play a role in the regulation of cellular growth and in signal transduction pathways. It is reported that ANXA10 may be a clinical relevant marker for predicting outcome in both early and advanced stages of bladder cancer.

CD164 was found to play a role in many malignant diseases. CD164 was associated with clinical and pathological features of patients. High level of CD164 was related to the distant metastasis and vascular invasion of bladder cancer patients.CD164 was associated with the poor clinical outcomes of BC patients. Silencing of CD164 could inhibit the progression of tumors in vivo and in vitro, which may become an effective target in the treatment of bladder cancer. CD164 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 41.2 kDa and the accession number is Q04900-1.

Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication.

HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family, and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is a rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin, and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Defects in HRAS are the cause of oral squamous cell carcinoma.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy

The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 64.8 kDa and the accession number is Q8IZJ1-1.

The netrin-1 receptor, UNC-5 Homology B, or UNC5B plays vital roles in angiogenesis, inflammation, embryonic development and carcinogenesis. Overexpression of UNC5B human colon epithelial cells suppressed dextran sodium sulfate, or DSS-induced apoptosis and caspase-3 activity. Besides, is a potential anti-neoplastic target in bladder cancer progression and inflammatory arthritis. UNC5B Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 39.2 kDa and the accession number is Q8IZJ1-1.

Gastric cancer is a deadly malignancy and is a prognostically unfavorable entity with restricted therapeutic strategies available. Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein widely expressed in bladder, prostate, and pancreatic cancers. Existing studies have thoroughly recognized the availability of utilizing anti-PSCA CAR-T cells in the treatment of metastatic prostate cancer and non-small-cell lung cancer. PSCA Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 34.3 kDa and the accession number is O43653.

Gastric cancer is a deadly malignancy and is a prognostically unfavorable entity with restricted therapeutic strategies available. Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein widely expressed in bladder, prostate, and pancreatic cancers. Existing studies have thoroughly recognized the availability of utilizing anti-PSCA CAR-T cells in the treatment of metastatic prostate cancer and non-small-cell lung cancer. PSCA Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 34.5 kDa and the accession number is P57096.