Deleted in malignant brain tumors 1 protein, also known as glycoprotein 34, surfactant pulmonary-associated D-binding protein, DMBT1 and GP34, is a secreted protein which belongs to theDMBT1 family. DMBT1 contains 2CUB domains, 14SRCR domains and 1ZP domain. It is highly expressed in alveolar and macrophage tissues. In some macrophages, expression is detected on the membrane, and in other macrophages, it is strongly expressed in the phagosome/phagolysosome compartments. Defects in DMBT1 are involved in the development of glioma (GLM). Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas , and ependymomas. DMBT1 may be considered as a candidate tumor suppressor for brain, lung, esophageal, gastric, and colorectal cancers. It may play roles in mucosal defense system, cellular immune defense and epithelial differentiation. DMBT1 may play a role as an opsonin receptor for SFTPD and SPAR in macrophage tissues throughout the body, including epithelial cells lining the gastrointestinal tract. It may be an important factor in fate decision and differentiation of transit-amplifying ductular (oval) cells within the hepatic lineage. DMBT1 may function as a binding protein in saliva for the regulation of taste sensation. It binds to HIV-1 envelope protein and has been shown to both inhibit and facilitate viral transmission.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

PRAME (PReferentially expressed Antigen in MElanoma) is a melanoma-associated antigen expressed in cutaneous and ocular melanomas and some other malignant neoplasms, while its expression in normal tissue and benign tumors is limited.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

Seizure-related 6 homolog (mouse)-like 2 (SEZ6L2) was shown to be involved in transcription of a type 1 transmembrane protein for regulating cell fate. SEZ6L2 was significantly up-regulated in tumour tissues of patients with CRC compared with adjacent normal tissues. Up-regulation of SEZ6L2 was correlated with a poor prognosis in patients with CRC. Furthermore, SEZ6L2 expression was inversely correlated with the expression of cytochrome C in malignant tissues in patients with CRC.

CD98 is a multifunctional glycoprotein that is involved in various biological processes such as amino acid transport, cell adhesion, diffusion, adhesion, and proliferation. CD98 can interact with CD147 to induce integrin 1 function to promote cyclosporine B-induced cell adhesion and p44/p42 MAPK activation following PI3K activation. CD98 heavy chain has been studied to be a key player in tumorigenesis due to its role in activating integrin signaling to promote tumor progression via angiogenesis, invasiveness, and proliferation in addition to promoting malignant transformation of cells. Fibrotic progression in the liver could be linked to the activation of integrin αvβ1 via CD98. CD98’s role in T cell activation in which the TGF activation could also play a profibrotic role.

Sorbitol dehydrogenase, also known as L-iditol 2-dehydrogenase and SORD, is a member of the zinc-containing alcohol dehydrogenase family. SORD exsits in a homotetramer and binds one zinc ion per subunit. SORD is expressed in kidney and epithelial cells of both benign and malignant prostate tissue. SORD can converts sorbitol to fructose and catalyzes the interconversion of polyols and their corresponding ketoses, and together with aldose reductase to make up the sorbitol pathway. SORD is up-regulated by androgens and down-regulated by castration. SORD may play a role in the sperm motility by providing an energetic source for sperm.

FcRH5 is a cell surface marker enriched on malignant plasma cells when compared to other hematologic malignancies and normal tissues. DFRF4539A is an anti-FcRH5 antibody-drug conjugated to monomethyl auristatin E (MMAE), a potent anti-mitotic agent. FcRH5/FcRL5 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with N-His-Avi tag. The predicted molecular weight is 94.19 kDa and the accession number is Q96RD9-1.

Protein S100-A7, also known as S100 calcium-binding protein A7, Psoriasin, S100A7, and PSOR1, is a secreted protein which belongs to theS-100 family. S100A7 was first isolated from skin involved by psoriasis, which can be induced in cultured squamous epithelial cells. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype.

Koebnerisin is also known as protein S100-A7A (S100A7A), S100 calcium-binding protein A7-like 1 (S100A7L1) or S100 calcium-binding protein A15 (S100A15). Human S100A7A / S100A15 is a novel member of the S100 family of EF-hand calcium-binding proteins and was recently identified in psoriasis, where it is significantly upregulated in lesional skin. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype. The association of the 11.2 kDa S100A7A / S100A15 with psoriasis suggests that it contributes to the pathogenesis of the disease and could provide a molecular target for therapy.

Telomeric repeat binding factor 1 (TRF1), also known as TERF1, the shelterin complex, which modulates the telomere structures. TRF1 protein structure contains a C-terminal Myb motif, a dimerization domain near its N-terminus and an acidic N-terminus. Pin2/TRF1 was originally identified as a protein bound to telomeric DNA (TRF1) and as a protein involved in mitotic regulation (Pin2). Pin2/TRF1 negatively regulates telomere length and importantly, its function is tightly regulated during the cell cycle, acting as an important regulator of mitosis. TRF1 can be bound and modulated by two nucleolar GTP-binding proteins, nucleostemin (NS) and guanine nucleotide binding protein-like 3-like (GNL3L), which exhibit apparently opposite effects on the protein degradation of TRF1. TRF1/TERF1 may has associated with cancer. TRF1 may play a significant role in cell differentiation in non-small cell lung cancer (NSCLC). The expression level of TRF1 protein is significantly reduced in kidney cancer and the level is negatively correlated with malignant degree of the cancer. TRF1 expression in malignant gliomas cells, may play a role in the malignant progression of astroglial brain tumors.

RELA (v-rel reticuloendotheliosis viral oncogene homolog A), also known as Nuclear factor NF-kappa-B p65 subunit, or Transcription factor p65, is a transcription factor expressed in growth plate chondrocytes where it facilitates chondrogenesis. The v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA) gene encodes the major component of the NF-?B complex. NF-kappaB is a generic name for an evolutionarily conserved transcription-factor system that contributes to the mounting of an effective immune response but is also involved in the regulation of cell proliferation, development, and apoptosis. The implication of NF-kappaB in central biological processes and its extraordinary connectivity to other signaling pathways raise a need for highly controlled regulation of NF-kappaB activity at several levels. The mammalian Rel/NF-kappaB family of transcription factors, including RelA, c-Rel, RelB, NF-kappaB1 (p50 and its precursor p105), and NF-kappaB2 (p52 and its precursor p100), plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation.

Jumping translocation breakpoint, also known as JTB, is a member of the JTB family. Jumping translocation (JT) is an unbalanced translocation that comprises amplified chromosomal segments jumping to various telomeres. JTB is expressed in all normal human tissues studied but overexpressed or underexpressed in many of their malignant counterparts. It is required for normal cytokinesis during mitosis. JTB plays a role in the regulation of cell proliferation. It may be a component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly.

Human papillomavirus (HPV) 16 infection is a necessary condition for the pathogenesis and development of cervical cancer. The E6 protein is expressed by the HPV16 E6 gene and promotes malignant phenotype transformation, which is an important mechanism for the occurrence and development of cervical cancer.

PRAME (PReferentially expressed Antigen in MElanoma) is a melanoma-associated antigen expressed in cutaneous and ocular melanomas and some other malignant neoplasms, while its expression in normal tissue and benign tumors is limited.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

ATP-binding cassette sub-family B member 5(ABCB5) is a plasma membrane-spanning protein. ABCB5 is principally expressed in physiological skin and human malignant melanoma. ABCB5 has been suggested to regulate skin progenitor cell fusion and mediate chemotherapeutic drug resistance in stem-like tumor cell subpopulations in human malignant melanoma. It is commonly over-expressed on circulating melanoma tumour cells. Furthermore, the ABCB5+ melanoma- initiating cells were demonstrated to express FLT1 (VEGFR1) receptor tyrosine kinase which was functionally required for efficient xenograft tumor formation, as demonstrated by shRNA knockdown experiments.

BLOC1S2 (Biogenesis of lysosome-related organelles complex-1 subunit 2) protein is widely expressed in normal tissue as well as in malignant tumors with a tendency towards lower expression levels in certain subtypes of tumors. On the subcellular level, BLOC1S2 is expressed in an organellar-like pattern and co-localizes with mitochondria.

The interplay between glioma stem cells (GSCs) and the tumor microenvironment plays crucial roles in promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor. WISP1 is preferentially expressed and secreted by GSCs. Silencing WISP1 markedly disrupts GSC maintenance, reduces tumor-supportive TAMs (M2), and potently inhibits GBM growth. WISP1 signals through Integrin α6β1-Akt to maintain GSCs by an autocrine mechanism and M2 TAMs through a paracrine manner.

Fibroblast activation protein (FAP) is a serine protease that has been reported in fibroblasts and some carcinoma cells, which correlates with poor patient outcomes. FAP can be induced under hypoxia which is also vital in the malignant behaviors of cancer cells. FAP Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 112.3 kDa and the accession number is Q12884-1.

Gastrokine 1 (GKN1) belongs to the BRICHOS domain family and plays a major role in maintaining gastric mucosa integrity. GKN1 is highly expressed in gastric tissue and is secreted into the stomach but is not expressed in gastric cancer. GKN1-mediated inhibition of APP processing might represent a new approach for the prevention and therapy of Alzheimer's disease (AD). In the presence of GKN2, GKN1 loses its ability to decrease cell proliferation, induce apoptosis, and inhibit epigenetic alterations in gastric cancer cells, that GKN2 may contribute to the homeostasis of gastric epithelial cells by inhibiting GKN1 activity. The loss of GKN1 function contributes to malignant transformation and proliferation of gastric epithelial cells in gastric carcinogenesis.

Aldo-keto reductases comprise of AKR1C1-AKR1C4, four enzymes that catalyze NADPH dependent reductions and have been implicated in biosynthesis, intermediary metabolism, and detoxification. there is a strong correlation between the expression levels of these family members and the malignant transformation as well as the resistance to cancer therapy. Type I human hepatic 3alpha-hydroxysteroid dehydrogenase (AKR1C4) plays a significant role in bile acid biosynthesis, steroid hormone metabolism, and xenobiotic metabolism.

Chloride intracellular channel protein 4, also known as Intracellular chloride ion channel protein p64H1 and CLIC4, is a member of the chloride channel CLIC family. It contains oneGST C-terminal domain. CLIC4 is a member of a family of intracellular chloride channels. It is regulated by p53, c-Myc, and tumor necrosis factor-alpha. CLIC4 is detected in epithelial cells from colon, esophagus and kidney (at protein level). CLIC4 has alternate cellular functions like a potential role in angiogenesis or in maintaining apical-basolateral membrane polarity during mitosis and cytokinesis. CLIC4 could promote endothelial cell proliferation and regulate endothelial morphogenesis (tubulogenesis). Expression of CLIC4 is prominent in heart, kidney, placenta and skeletal muscle. Overexpression of CLIC4 in cancer cells inhibits tumor growth. Conversely, overexpression of CLIC4 in tumor stromal cells stimulates tumor growth. Thus, CLIC4 participates in normal and pathological processes and may serve as a useful target for therapies in disturbances of homeostasis and neoplastic transformation. Loss of CLIC4 in tumor cells and gain in tumor stroma is common to many human cancers and marks malignant progression. Up-regulation of CLIC4 in tumor stroma is coincident with myofibroblast conversion, generally a poor prognostic indicator. Reactivation and restoration of CLIC4 in tumor cells or the converse in tumor stromal cells could provide a novel approach to inhibit tumor growth.

SERPINB3, also known as SCCA-1, belongs to the serpin family. Serpins are a group of proteins with similar structures that were first identified as a set of proteins able to inhibit proteases. The acronym serpin was originally coined because many serpins inhibit chymotrypsin-like serine proteases. SERPINB3 is expressed in some hepatocellular carcinoma (at protein level). Its expression is closely related to cellular differentiation in both normal and malignant squamous cells. It seems to also be secreted in plasma by cancerous cells but at a low level. SERPINB3 significantly attenuates apoptosis by contrasting cytochrome c release from the mitochondria and by antichemotactic effect for NK cells. It may act as a protease inhibitor to modulate the host immune response against tumor cells and may be involved in the malignant behavior of squamous cell carcinoma cells.

PRAME (PReferentially expressed Antigen in MElanoma) is a melanoma-associated antigen expressed in cutaneous and ocular melanomas and some other malignant neoplasms, while its expression in normal tissue and benign tumors is limited.

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.

Melanoma Inhibitory Activity Protein (MIA) is an autocrine growth regulatory protein secreted from chondrocytes and malignant melanoma cells, which was the first discovered member of a family of secreted cytokines termed the MIA/OTOR family. The four known members of this family: MIA, MIA2, OTOR and TANGO each contain a Src homology-3 (SH3)-like domain. MIA acts as a potent tumor cell growth inhibitor for malignant melanoma cells and some other neuroectodermal tumors, including gliomas, in an autocrine fashion and promotes melanoma metastasis by binding competitively to fibronectin and laminin in a manner that results in melanoma cell detachment from the extracellular matrix in vivo. The protein MIA has been shown to represent a very sensitive and specific serum marker for systemic malignant melanoma that might be useful for staging of primary melanomas, detection of progression from localized to metastatic disease during follow-up, and monitoring therapy of advanced melanomas. Elevated levels of MIA may represent a clinically useful marker for diagnosis of melanoma metastasis as well as a potential marker for rheumatoid arthritis.

FcRH5 is a cell surface marker enriched on malignant plasma cells when compared to other hematologic malignancies and normal tissues. DFRF4539A is an anti-FcRH5 antibody-drug conjugated to monomethyl auristatin E (MMAE), a potent anti-mitotic agent. FcRH5/FcRL5 Protein (Primary Amine Labeling), Human, Recombinant (His), Biotinylated is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 92.38 kDa and the accession number is AAK93971.

Protein-arginine deiminase type-4, also known as HL-6 PAD, Peptidylarginine deiminase IV, Protein-arginine deiminase type I V and PADI4, is a cytoplasm and nucleus protein that belongs to the protein arginine deiminase family. PADI4 is expressed in CD34+stem cells in normal tissues, and many more CD34+ cells expressing PADI4 are present in tumour tissues. PADI4 post-translationally converts peptidylarginine to citrulline, a process called citrullination. Studies have demonstrated the high expression of PADI4 in various malignant tumor tissues. PADI4 is also expressed at high levels in the blood of patients with some malignant tumors. Citrullination of histone, cytokeratin, antithrombin and fibronectin have been confirmed to be involved in abnormal apoptosis, high coagulation, and disordered cell proliferation and differentiation, all of which are main features of malignant tumors. PADI4 may play an important role in tumorigenesis. Genetic variations in PADI4 are a cause of susceptibility to rheumatoid arthritis (RA). It is a systemic inflammatory disease with autoimmune features and a complex genetic component. It primarily affects the joints and is characterized by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures.

Folate receptor beta, also known as Folate receptor 2, FBP, and FOLR2, is a member of the folate receptor family. FOLR2 is expressed in placenta and hematopoietic cells. The expression of FOLR2 is increased in malignant tissues. Members of the Folate receptor family members (FOLRs) have a high affinity for folic acid and for several reduced folic acid derivatives. They mediate the delivery of 5-methyltetrahydrofolate to the interior of, out of within, or between cells in a process known as potocytosis. FOLR2 has a 68% and 79% sequence homology with the FOLR1 and FOLR3 proteins, respectively. The FOLR2 protein was originally thought to exist only in placenta, but is also detected in spleen, bone marrow, and thymus. FOLR2 is a marker for macrophages generated in the presence of M-CSF, but not GM-CSF. Its expression correlates with increased folate uptake ability. Folate conjugates of therapeutic drugs are a potential immunotherapy tool to target tumor-associated macrophages.

Death-associated protein kinase 1, also known as DAP kinase 1, DAPK1 and DAPK, is a cytoplasm protein which belongs to theprotein kinase superfamily, CAMK Ser / Thr protein kinase family and DAP kinase subfamily. DAPK1 contains tenANK repeats, onedeath domain and oneprotein kinase domain. DAPK1 is a calcium / calmodulin-dependent serine/threonine kinase which acts as a positive regulator of apoptosis. DAPK1 gene is a candidate tumor suppressor (TSG) and the abnormal methylation of DAPK1 gene has been found in many carcinomas. DAPK1 over-expression can induce cell apoptosis and inhibit tumor cell metastasis. DAPK1 gene over-expression could suppress PGCl3 cells malignant phenotype, inhibit PGCl3 cells growth, invasive, migration and adhesion ability, upregulate p53 gene and downregulate bcl-2 gene. Loss of activity of death-associated protein kinase 1 ( DAPK1 ) may be an independent factor affecting survival of non-small cell lung cancer patients. DAPK1 promoter methylation might play a significant role in the progression of chronic myeloid leukemia ( CML ).

LAP3 (Leucine Aminopeptidase 3) is a Protein Coding gene. 2 alternative initiation human isoforms have been reported. LAP3, belonging to the peptidase M17 family, has been proved to catalyze the hydrolysis of leucine residues. It catalyzes the removal of unsubstituted N-terminal amino acids from various peptides and is presumably involved in the processing and regular turnover of intracellular proteins. Leucine aminopeptidases are involved in many pathological disorders and regulate cell proliferation, invasion, and/or angiogenesis of tumors. A recent study showed that LAP3 is highly expressed in several malignant and affects tumor angiogenesis. LAP3 is widely expressed in the appendix, lymph node, and other tissues. Diseases associated with LAP3 include Bacterial Vaginosis and Trichomoniasis.

RNF43 mutations are frequently detected in colorectal cancer cells and lead to a loss of function of the ubiquitin E3 ligase. The outer mitochondrial membrane 34 (TOMM34) and ring finger protein 43 (RNF43) as highly expressed oncogenes in malignant colorectal tumors. RNF43 is a tumour suppressor gene that suppresses the Wnt-beta-catenin signalling pathway. RNF43 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 45.8 kDa and the accession number is Q68DV7-1.

DCUN1D1, also known as SCCRO, is part of an E3 ubiquitin ligase complex for neddylation. DCUN1D1 functions to recruit charged E2 and is involved in the release of inhibitory effects of CAND1 on cullin-RING ligase E3 complex assembly and activity. DCUN1D1 binds to the components of the neddylation pathway (Cullin-ROC1, Ubc12, and CAND1) and augments but is not required for cullin neddylation in reactions using purified recombinant proteins. DCUN1D1 also recruits Ubc12 approximately NEDD8 to the CAND1-Cul1-ROC1 complex but that this is not sufficient to dissociate or overcome the inhibitory effects of CAND1 on cullin neddylation in purified protein assays. DCUN1D1 also acts as am ncogene facilitating malignant transformation and carcinogenic progression.

MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. Myeloperoxidase (MPO) is an important enzyme, which is one of the components of the antibacterial system in neutrophils and monocytes. MPO participates in the inflammatory response in multiple locations in the body, including the mammary glands. Myeloperoxidase (MPO), a specific polymorphonuclear leukocyte enzyme, has been used previously to quantify the number of neutrophils in tissue. MPO activity was found to be linearly related to the number of neutrophil cells. The MPO system plays an important role in the control of infections and the deletion of malignant cells. Nevertheless, alternations in the MPO system can lead to DNA damage and carcinogenesis. Polymorphisms in the MPO gene have been associated with an increased expression of MPO and a higher risk for the development of cancer. Myeloperoxidase (MPO) is one of the major target antigens of antineutrophil cytoplasmic autoantibodies (ANCA) found in patients with small-vessel vasculitis and Pauci-immune necrotizing glomerulonephritis. Myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) is an autoantibody that is frequently found in patients with vasculitides.

Human papillomavirus (HPV) 16 infection is a necessary condition for the pathogenesis and development of cervical cancer. The E6 protein is expressed by the HPV16 E6 gene and promotes malignant phenotype transformation, which is an important mechanism for the occurrence and development of cervical cancer.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

The immunoproteasome, having been linked to neurodegenerative diseases and hematological cancers, has been shown to play an important role in MHC class I antigen presentation. The development of molecular probes that selectively inhibit the major catalytic subunit, LMP2, of the immunoproteasome,LMP2-rich cancer cells compared to LMP2-deficient cancer cells are more sensitive to growth inhibition by the LMP2-specific inhibitor, implicating an important role of LMP2 in regulating cell growth of malignant tumors that highly express LMP2.

Fibroblast activation protein (FAP) is a serine protease that has been reported in fibroblasts and some carcinoma cells, which correlates with poor patient outcomes. FAP can be induced under hypoxia which is also vital in the malignant behaviors of cancer cells. FAP Protein, Cynomolgus, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with N-His-Avi tag. The predicted molecular weight is 88 kDa and the accession number is A0A2K5VGF4.

The chondroitin sulfate proteoglycan-4 (CSPG4) is a cell surface proteoglycan overexpressed in a huge range of human and canine neoplastic lesions by tumor cells, tumor microenvironment and cancer initiating cells. CSPG4 plays a central role in the oncogenic pathways required for malignant progression and metastatization.

FcRH5 is a cell surface marker enriched on malignant plasma cells when compared to other hematologic malignancies and normal tissues. DFRF4539A is an anti-FcRH5 antibody-drug conjugated to monomethyl auristatin E (MMAE), a potent anti-mitotic agent. FcRH5/FcRL5 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 53.7 kDa and the accession number is Q68SN8-1.

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.

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of CD5 B lymphocytes in peripheral blood, lymphoid organs and bone marrow. The main feature of the disease is accumulation of the malignant cells due to decreased apoptosis. CD84 belongs to the signaling lymphocyte activating molecule family of immunoreceptors, and has an unknown function in CLL cells.

Glutamate decarboxylase 1, also known as 67 kDa glutamic acid decarboxylase, Glutamate decarboxylase 67 kDa isoform and GAD1, is a member of thegroup II decarboxylase family. GAD1 is expressed in benign and malignant prostatic tissue and may serve as a highly prostate-specific tissue biomarker. GAD1 isoform3 is expressed in pancreatic islets, testis, adrenal cortex, and perhaps other endocrine tissues, but not in brain. Tissue-specific markers are useful for identification of tumour type in advanced cancers of unknown origin. In plants, as in most eukaryotes, glutamate decarboxylase catalyses the synthesis of GABA. Root-specific calcium/calmodulin-regulated GAD1 plays a major role in GABA synthesis in plants under normal growth conditions and in response to stress. Defects in GAD1 are the cause of cerebral palsy spastic quadriplegic type 1 (CPSQ1)which is a non-progressive disorder of movement and/or posture resulting from defects in the developing central nervous system. Affected individuals manifest symmetrical, non-progressive spasticity and no adverse perinatal history or obvious underlying alternative diagnosis.

NEK3 (NIMA (never in mitosis gene a)-related expressed kinase 3), contains 1 protein kinase domain and is a member of the NimA (never in mitosis A) family of serine/threonine protein kinases. Members of the NEK family of protein kinases share high amino acid homology with NIMA (never in mitosis gene a). NEK3 differs from other NimA family members in that it is not the cell cycle-regulated and is found primarily in the cytoplasm. It is activated by prolactin stimulation, leading to phosphorylation of VAV2 guanine nucleotide exchange factor, paxillin, and activation of the RAC1 GTPase. NEK3 mRNA can be detected in all the proliferating cell lines with the amount not changing during the cell cycle. Prolactin stimulates interaction between NEK3 and paxillin leading to increased paxillin phosphorylation, Analysis of breast tissue microarrays show a significant up-regulation of NEK3 expression in malignant versus normal specimens. Multiple transcript variants encoding different isoforms have been found for the NEK3 gene. NEK3 may play a role in mitotic regulation.

RNF43 mutations are frequently detected in colorectal cancer cells and lead to a loss of function of the ubiquitin E3 ligase. The outer mitochondrial membrane 34 (TOMM34) and ring finger protein 43 (RNF43) as highly expressed oncogenes in malignant colorectal tumors. RNF43 is a tumour suppressor gene that suppresses the Wnt-beta-catenin signalling pathway. RNF43 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 20.5 kDa and the accession number is Q68DV7-1.

PFKP plays a critical role in cell proliferation in breast cancer cells. PFKP is necessary for starvation-mediated autophagy, glycolysis, and EMT, thereby promoting the malignant progression of OSCC. The Snail-PFKP axis plays an important role in cancer cell survival via regulation of glucose flux between glycolysis and PPP.

PRAME (PReferentially expressed Antigen in MElanoma) is a melanoma-associated antigen expressed in cutaneous and ocular melanomas and some other malignant neoplasms, while its expression in normal tissue and benign tumors is limited.

PRAME (PReferentially expressed Antigen in MElanoma) is a melanoma-associated antigen expressed in cutaneous and ocular melanomas and some other malignant neoplasms, while its expression in normal tissue and benign tumors is limited.