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Anti-GHRL Rabbit Polyclonal Antibody

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Anti-Red Blood Cells Rabbit Polyclonal Antibody

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Anti-LAMA1 Rabbit Polyclonal Antibody

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Receptor for EGF, but also for other members of the EGF family, as TGF-alpha, amphiregulin, betacellulin, heparin-binding EGF-like growth factor, GP30 and vaccinia virus growth factor. Is involved in the control of cell growth and differentiation. Phosphorylates MUC1 in breast cancer cells and increases the interaction of MUC1 with SRC and CTNNB1/beta-catenin.

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Anti-UBC Rabbit Polyclonal Antibody

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Anti-PARK7 Rabbit Polyclonal Antibody

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Anti-STK38 Mouse Monoclonal Antibody

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Anti-TNF Mouse Monoclonal Antibody

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Anti-ERP44 Mouse Monoclonal Antibody

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Anti-NOTCH4 Mouse Monoclonal Antibody

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Anti-BAG1 Mouse Monoclonal Antibody

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Anti-PTPRC Mouse Monoclonal Antibody

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Anti-NEIL3 Rabbit Polyclonal Antibody

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Anti-GPX1 Rabbit Polyclonal Antibody

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Anti-SMURF1 Rabbit Polyclonal Antibody

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NF-κ-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κ-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-κ-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-κ-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-κ-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-κ-B complex which translocates to the nucleus. NF-κ-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-κ-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-κ-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-κ-B complex

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The protein encoded by Cyclin B1 is a regulatory protein involved in mitosis. The gene product complexes with p34(cdc2) to form the maturation-promoting factor (MPF). Two alternative transcripts have been found, a constitutively expressed transcript and a cell cycle-regulated transcript, that is expressed predominantly during G2/M phase. The different transcripts result from the use of alternate transcription initiation sites.

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Participates in the Wnt signaling pathway. Implicated in the hormonal control of several regulatory proteins including glycogen synthase, MYB and the transcription factor JUN. Phosphorylates JUN at sites proximal to its DNA-binding domain, thereby reducing its affinity for DNA. Phosphorylates MUC1 in breast cancer cells, and decreases the interaction of MUC1 with CTNNB1/beta-catenin. Phosphorylates CTNNB1/beta-catenin.

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Anti-HSP90AA1 Mouse Monoclonal Antibody

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Anti-ID3 Rabbit Polyclonal Antibody

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Anti-PARP1 Rabbit Polyclonal Antibody

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Anti-SYP Rabbit Polyclonal Antibody

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Anti-TGFBR3 Rabbit Polyclonal Antibody

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Anti-SENP1 Rabbit Polyclonal Antibody

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Anti-LIMK1 Mouse Monoclonal Antibody

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BCL-2 encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends.

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Signal transducer and activator of transcription that mediates signaling by interferons (IFNs). Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state.

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Transcription factor that binds to the interleukin-6 (IL-6)-responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA.

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Anti-SOX9 Rabbit Polyclonal Antibody

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Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3'), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2-c-Jun complex.