Phospho-PRKCZ (T560) Recombinant Monoclonal Antibody

Shipped with Ice Packs
In Stock
Cat. No.
BT2012002
Synonyms
14-3-3-zetaisoform antibody; AI098070 antibody; aPKCzeta antibody; C80388 antibody; EC 2.7.11.13 antibody; KPCZ_HUMAN antibody; nPKC zeta antibody; nPKC-zeta antibody; OTTHUMP00000001368 antibody; OTTHUMP00000044160 antibody; PKC 2 antibody; PKC ZETA antibody; PKC2 antibody; Pkcz antibody; PKCZETA antibody; PKM-zeta; included antibody; PRKCZ antibody; Protein kinase C zeta antibody; Protein kinase C zeta form antibody; Protein kinase C zeta type antibody; r14-3-3 antibody; R74924 antibody; zetaPKC antibody
Quick Inquiry

Description

Biological Relevance of PRKCZ

PRKCZ is an atypical protein kinase C isoform that regulates:

  • Cell signaling: PI3K/AKT, ERK/MAPK, and NF-κB pathways .

  • Cellular processes: Proliferation, survival, motility, and maintenance of long-term potentiation (LTP) .

  • Disease links: Ovarian tumorigenesis (via IGF1R/ITGB3 pathways) , asthma (Th2 immune response) , and insulin signaling (GLUT4 translocation) .

Key functional insights:

  • Phosphorylates RELA at Ser311 to relieve NF-κB repression .

  • Activates JAK1/STAT6 in Th2 differentiation .

  • Associates with PARD6A/CDC42 to establish cell polarity .

3.1. Western Blot Validation

  • Detects endogenous PRKCZ phosphorylation in A549 cell lysates .

  • Sensitivity confirmed using secondary goat anti-rabbit IgG (1:50,000 dilution) .

3.2. Disease Models

  • Cancer: PRKCZ promotes tumor progression via ERK/MAPK and NF-κB activation .

  • Neurology: Maintains LTP in hippocampal neurons .

  • Inflammation: Required for LPS-induced macrophage signaling .

3.3. Comparative Performance

  • Clone 1B10 (Cusabio/Abnova) shows higher specificity for human samples vs. clone EP2037AY (Abcam), which cross-reacts with rodents .

  • Commercial antibodies (e.g., Sigma-Aldrich’s GED-16) prioritize phosphorylation-specific detection .

Validation and Citations

  • Cusabio/Abnova: Validated in WB using A549 lysates .

  • Abcam (ab62372): Cited in 22 publications, including phospho-specific assays .

  • Sigma-Aldrich: Optimized for IHC (1:50–1:200) and WB (1:1000–1:2000) .

Critical Considerations

  • Sodium azide: Present in storage buffers; requires careful handling .

  • Phospho-specificity: Confirmed via Mps1 kinase inhibition assays in analogous antibodies .

  • Storage: Long-term stability at -80°C; avoid glycerol crystallization .

Emerging Research Directions

  • Therapeutic targeting: PRKCZ inhibition in ovarian cancer .

  • Neuronal plasticity: Role in Alzheimer’s models via LTP modulation .

  • Structural studies: Cryo-EM analysis of PRKCZ-kinase complexes .

Product Specs

Buffer
Rabbit IgG in phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Description

The coding sequence for the phospho-PRKCZ (T560) monoclonal antibody, isolated by immunizing animals with human pT560-PRKCZ, was cloned into plasmids and subsequently transfected into cell lines for in vitro expression. The product was purified using affinity chromatography, resulting in the phospho-PRKCZ (T560) recombinant monoclonal antibody. This anti-pT560-PRKCZ antibody is a rabbit IgG, specifically designed for the detection of human PRKCZ phosphorylated at Thr 560 residue. It is suitable for use in ELISA and Western Blot applications.

PRKCZ, an atypical protein kinase C isoform, plays a crucial role in regulating diverse signaling events, including cell proliferation, survival, and motility. These processes are critical for cancer development and progression. PRKCZ participates in various signaling pathways, such as the activation of the ERK/MAPK cascade, the p70 ribosomal S6 kinase signaling cascade, the transcription factor NF-κB, and cell polarity regulation. Kelly K. Y. Seto et al. discovered that PRKCZ is a promising regulatory component of the IGF1R and ITGB3 pathways, suggesting its potential significance in ovarian tumorigenesis.

Form
Liquid
Lead Time
Typically, we are able to ship products within 1-3 business days after receiving your orders. Delivery time may vary depending on the mode of purchase or location. For specific delivery timeframes, please consult your local distributors.
Synonyms
14-3-3-zetaisoform antibody; AI098070 antibody; aPKCzeta antibody; C80388 antibody; EC 2.7.11.13 antibody; KPCZ_HUMAN antibody; nPKC zeta antibody; nPKC-zeta antibody; OTTHUMP00000001368 antibody; OTTHUMP00000044160 antibody; PKC 2 antibody; PKC ZETA antibody; PKC2 antibody; Pkcz antibody; PKCZETA antibody; PKM-zeta; included antibody; PRKCZ antibody; Protein kinase C zeta antibody; Protein kinase C zeta form antibody; Protein kinase C zeta type antibody; r14-3-3 antibody; R74924 antibody; zetaPKC antibody
Target Names
PRKCZ
Uniprot No.
Q05513

Target Background

Function
Calcium- and diacylglycerol-independent serine/threonine-protein kinase that functions within the phosphatidylinositol 3-kinase (PI3K) pathway and mitogen-activated protein (MAP) kinase cascade, and is involved in NF-κB activation, mitogenic signaling, cell proliferation, cell polarity, inflammatory response, and maintenance of long-term potentiation (LTP). Upon lipopolysaccharide (LPS) treatment in macrophages, or following mitogenic stimuli, functions downstream of PI3K to activate MAP2K1/MEK1-MAPK1/ERK2 signaling cascade independently of RAF1 activation. Required for insulin-dependent activation of AKT3, but may function as an adapter rather than a direct activator. Upon insulin treatment may act as a downstream effector of PI3K and contribute to the activation of translocation of the glucose transporter SLC2A4/GLUT4 and subsequent glucose transport in adipocytes. In EGF-induced cells, binds and activates MAP2K5/MEK5-MAPK7/ERK5 independently of its kinase activity and can activate JUN promoter through MEF2C. Through binding with SQSTM1/p62, functions in interleukin-1 signaling and activation of NF-κB with the specific adapters RIPK1 and TRAF6. Participates in TNF-dependent transactivation of NF-κB by phosphorylating and activating IKBKB kinase, which in turn leads to the degradation of NF-κB inhibitors. In migrating astrocytes, forms a cytoplasmic complex with PARD6A and is recruited by CDC42 to function in the establishment of cell polarity along with the microtubule motor and dynein. In association with FEZ1, stimulates neuronal differentiation in PC12 cells. In the inflammatory response, is required for the T-helper 2 (Th2) differentiation process, including interleukin production, efficient activation of JAK1 and the subsequent phosphorylation and nuclear translocation of STAT6. May be involved in development of allergic airway inflammation (asthma), a process dependent on Th2 immune response. In the NF-κB-mediated inflammatory response, can relieve SETD6-dependent repression of NF-κB target genes by phosphorylating the RELA subunit at 'Ser-311'. Phosphorylates VAMP2 in vitro; Involved in late synaptic long term potention phase in CA1 hippocampal cells and long term memory maintenance.
Gene References Into Functions
  1. PKCzeta promoted lung adenocarcinoma invasion and metastasis, and its expression was associated with MMP2 and MMP9 expression. PMID: 28983601
  2. PKC-zeta may be responsible for the abnormal growth, proliferation, and migration of metastatic LOVO colon cancer cells via PKC-zeta/Rac1/Pak1/beta-Catenin pathway. PMID: 29408512
  3. reduced expression of PKCzeta/Pard3/Pard6 contributes to non-small-cell lung cancer epithelial-mesenchymal transition, invasion, and chemoresistance. PMID: 28652146
  4. Intestinal I/R induced the membrane translocation and phosphorylation of PKCzeta. Pretreatment with the PKCzeta activator phosphatidylcholine remarkably attenuated gut injury by suppressing apoptosis. H/R induced PKCzeta to combine with TRAF2, which was phosphorylated by PKCzeta at Ser(55), but not at Ser(11), under intestinal I/R or H/R conditions PMID: 28726782
  5. these results conclude that miR-25 targets PKCzeta and protects osteoblastic cells from Dex via activating AMPK signaling. PMID: 27911275
  6. PKCzeta was specifically involved in ACOT7 depletion-mediated cell cycle arrest as an upstream molecule of the p53-p21 signaling pathway in MCF7 human breast carcinoma and A549 human lung carcinoma cells. PMID: 28518146
  7. we found that Wnt3a treatment rapidly induces hyperphosphorylation and stabilization of Dvl2 and Dvl3. Our findings suggest a model of positive regulation of PKCzeta-mediated Dvl signaling activity, to produce a strong and sustained response to Wnt3a treatment by stabilizing Dvl protein levels. PMID: 28366812
  8. The data demonstrate that PKCzeta expression regulates the maturation of neonatal T-cells into specific functional phenotypes and that environmental influences may work via PKCzeta to regulate these phenotypes and disease susceptibility. PMID: 28159873
  9. Drug discovery efforts have been hindered due to the non-availability of the protein structure and hence in the present study we attempted to build the open and closed models of the protein PKMzeta using homology modeling. PMID: 27490967
  10. This study demonstrated that zinc upregulates PKCzeta by activating GPR39 to enhance the abundance of ZO-1, thereby improving epithelial integrity in S. typhimurium-infected Caco-2 cells. PMID: 28515165
  11. Inhibition of protein kinase C zeta expression in prostate cancer cells promoted chemotaxis of peripheral macrophages and acquisition of M2 phenotypic features. These results were further supported by the finding that silencing of endogenous protein kinase C zeta promoted the expression of prostate cancer cell-derived interleukin-4 and interleukin-10 PMID: 28631559
  12. Here we provide the first evidence that PKC-zeta is a potential target for the treatment of COPD by selective small molecules PMID: 27516147
  13. Study provides evidence for a novel PKC-zeta to p47phox interaction that is required for cell transformation from blebbishields and ROS production in cancer cells. PMID: 27040869
  14. FRET-based translocation assays reveal that insulin promotes the association of both p62 and aPKC with the insulin-regulated scaffold IRS-1. PMID: 27143478
  15. data suggest that the interaction between this novel region in Galphaq and the effector PKCzeta is a key event in Galphaq signaling. PMID: 26887939
  16. The PKC-zeta - induced phosphorylation of GSK-3 beta stimulates GSK-3 beta activity. PMID: 26711256
  17. Over-expression of PRKCZ results in gene and/or protein expression alterations of insulin-like growth factor 1 receptor (IGF1R) and integrin beta 3 (ITGB3) in SKOV3 and OVCAR3 cells. PMID: 25874946
  18. PKCzeta inhibition prevented alternative cleavage and release of TROP2, suggesting that these events require endocytic uptake and exosomal release of the corresponding microvesicles. PMID: 25817572
  19. Data show that aPKC scaffold protein p62 tethers Atypical protein kinase C (aPKC) in an active conformation. PMID: 26187466
  20. PRKCZ methylation is associated with sunlight exposure PMID: 25075435
  21. Neuronal NF1/RAS regulation of cyclic AMP requires atypical PKC zeta activation, which is perturbed in neurofibromatosis type 1. PMID: 25070947
  22. The results indicate that induction and activation of PKCzeta promote TNBC growth, invasion and metastasis. PMID: 24786829
  23. PKCzeta and PKMzeta are overexpressed in TCF3-rearranged paediatric acute lymphoblastic leukaemia and may have a role in thiopurine sensitivity PMID: 24990612
  24. Results indicate that PKCzeta regulates survivin expression levels and inhibits apoptosis in colon cancer cells. PMID: 24920238
  25. These data indicate for the first time that HIV-1 Gag phosphorylation on Ser487 is mediated by atypical PKC and that this kinase may regulate the incorporation of Vpr into HIV-1 virions and thereby supports virus infectivity. PMID: 24447338
  26. STAT3 is an important downstream mediator of the pro-carcinogenic effects of PRKCZ in pancreatic cancer cells. PMID: 24015205
  27. Data indicate that both tumor focality and Par3/Par6/atypical protein kinase C (APKC) expression were significantly associated with tumor recurrence. PMID: 21549621
  28. Results indicate the importance of p62-associated PKCzeta in the overactive state of pagetic osteoclasts (OCs) and in the activation of NF-kappaB, particularly in the presence of the p62(P392L) mutation. PMID: 23266528
  29. The findings suggest a potential role for the use of PKCzeta levels in cord blood T cells as a presymptomatic test to predict allergy risk in children. PMID: 23004934
  30. Study reports that PKCzeta-deficient cells reprogram their metabolism for the utilization of glutamine instead of glucose through the serine biosynthetic cascade controlled by 3-phosphoglycerate dehydrogenase (PHGDH). PMID: 23374352
  31. It was concluded that protein kinase C zeta regulated protein kinase phosphorylation, which in turn regulated the proteolytic activity of phorbol dibutyrate-induced podosomes by influencing the recruitment of protein kinase C zeta and MMP9 to podosomes. PMID: 22740332
  32. A proapoptotic role for protein kinase C zeta in the binding and phosphorylating Bcl10 at the nuclear envelope. PMID: 22812606
  33. A novel sequence was identified within the 3'-terminal domain of human PRKCZ. PMID: 22644296
  34. these findings suggest that PKC-zeta is involved in the phosphorylation of HMGB1, and the phosphorylation of specific serine residues in the nuclear localization signal regions is related to enhanced HMGB1 secretion in colon cancer cells. PMID: 22750245
  35. Stat3 forms a multiprotein complex with Rac1 and PKC in an hypoxia-reoxygenation-dependent manner. PMID: 22791907
  36. Protein kinase C (PKC) zeta expression was significantly higher in normal than in cancerous tissues. Similarly, PKC zeta expression was down-regulated in four renal cancer cell lines compared to immortalized benign renal tubular cells. PMID: 22475628
  37. two key (hub) PPARgamma direct target genes, PRKCZ and PGK1, were experimentally validated to be repressed upon PPARgamma activation by its natural ligand, 15d-PGJ2 in three prostrate cancer cell lines PMID: 21780947
  38. The LNO(2) mediated signaling in lung type II epithelial cells occurs via a unique pathway involving PKCzeta. PMID: 21871968
  39. Western Blot data showed decreased expression (p < 0,05) of Munc18c and phospho-PKC Zeta in polycystic ovary-insulin resistant endometria (PCOSE-IR) with respect to the control. PMID: 22390153
  40. Single nucleotide polymorphisms in protein kinase C zeta are associated with bipolar affective disorder. PMID: 22231931
  41. Report role of PKC-zeta induction in bronchial inflammation and airyway hyperresponsiveness. PMID: 22324796
  42. HGF induced functional CXCR4 receptor expression in breast cancer cells. The effect of HGF was specifically mediated by PKCzeta activity. PMID: 22242160
  43. High levels of protein kinase C zeta expression were associated with lymphatic metastasis in squamous cervical cancer. PMID: 21895402
  44. Inhibition of protein kinase M zeta results in a reduction of synaptic PSD-95 accumulation in developing visual cortex PMID: 21849550
  45. Results indicate that phosphorylation of human DNMT1 by protein kinase C is isoform-specific and provides the first evidence of cooperation between PKCzeta and DNMT1 in the control of the DNA methylation patterns of the genome. PMID: 21619587
  46. human platelets express PKCzeta, and it may be constitutively phosphorylated at the activation loop threonine 410 and the turn motif threonine 560 under basal resting conditions, which are differentially dephosphorylated by outside-in signaling PMID: 21645497
  47. The PKCzeta activation by d-flow induces endothelial cell (EC) apoptosis by regulating p53. PMID: 21624955
  48. that upon DAMGO treatment, MOR activates PKCzeta through a PDK1-dependent signaling pathway to induce CCR5 phosphorylation and desensitization. PMID: 21454526
  49. The prognostic impact of TGF-beta1, NF-kappaB p105, PKC-zeta, Par-6alpha, E-cadherin and vimentin in non-gastrointestinal stromal tumor soft tissue sarcomas, was investigated. PMID: 21390241
  50. low levels of expression are associated with poorly differentiated tumours and a poor outcome in breast cancer patients PMID: 20844151

Show More

Hide All

Database Links

HGNC: 9412

OMIM: 176982

KEGG: hsa:5590

STRING: 9606.ENSP00000367830

UniGene: Hs.496255

Protein Families
Protein kinase superfamily, AGC Ser/Thr protein kinase family, PKC subfamily
Subcellular Location
Cytoplasm. Endosome. Cell junction. Membrane; Peripheral membrane protein.; [Isoform 2]: Cytoplasm.
Tissue Specificity
Expressed in brain, and to a lesser extent in lung, kidney and testis.

Q&A

What is PRKCZ and why is the phosphorylation at T560 significant?

Protein Kinase C zeta (PRKCZ) is a calcium- and diacylglycerol-independent serine/threonine-protein kinase that functions in multiple critical cellular pathways. It plays essential roles in:

  • Phosphatidylinositol 3-kinase (PI3K) signaling

  • Mitogen-activated protein (MAP) kinase cascade

  • NF-kappa-B activation

  • Mitogenic signaling and cell proliferation

  • Cell polarity establishment

  • Inflammatory response regulation

  • Maintenance of long-term potentiation (LTP)

Phosphorylation at threonine 560 (T560) represents a key post-translational modification that regulates PRKCZ activity. This site-specific phosphorylation is particularly important for the kinase's catalytic function and its ability to interact with downstream effectors in signaling cascades .

Sample preparation is critical for preserving phosphorylation status:

  • Immediate processing: Process tissues/cells immediately after collection to prevent phosphatase activity

  • Phosphatase inhibitors: Include phosphatase inhibitor cocktails in all lysis buffers

  • Cold chain maintenance: Keep samples at 4°C throughout processing

  • Lysis buffer composition: Use a buffer containing:

    • 150mM NaCl

    • Phosphate buffer (pH 7.4)

    • 0.02% sodium azide

    • Protease inhibitors

    • 50% glycerol for stability

  • Sonication protocol: Brief sonication (3×10s pulses) can improve extraction without denaturing phospho-epitopes

For Western blotting applications specifically, separate proteins on 10-12% SDS-PAGE gels and transfer to PVDF membranes for optimal binding of phospho-epitopes .

What controls should be included when using Phospho-PRKCZ (T560) antibodies?

Rigorous experimental design requires appropriate controls:

  • Positive control: A549 whole cell lysate has been validated as a positive control showing the expected 68 kDa band

  • Phosphatase treatment control: Treating duplicate samples with lambda protein phosphatase to abolish antibody binding

  • Loading control: Using pan-PRKCZ antibody on parallel blots to normalize phospho-signal

  • Isotype control: Using matched-isotype IgG for background assessment

  • Cross-reactivity control: Including samples from Prkcz knockout models when available to verify specificity

How can researchers verify antibody specificity?

Verifying antibody specificity is essential for reliable research outcomes:

  • Immunogen verification: Confirm the antibody was raised against a phospho-specific peptide corresponding to residues surrounding T560 of human PRKCZ

  • Predicted molecular weight: The expected molecular weight for PRKCZ is 68 kDa

  • Phosphatase treatment: Signal reduction after phosphatase treatment confirms phospho-specificity

  • Reactivity testing: Test across multiple species if working with non-human models (validated for human, mouse, rat)

  • Knockout validation: When possible, use Prkcz null samples as negative controls

How can researchers distinguish between PRKCZ phosphorylation and other closely related PKC isoforms?

Distinguishing PRKCZ phosphorylation from other PKC isoforms presents a significant challenge due to sequence homology, particularly with PKCι:

  • Cross-reactivity assessment: Test against recombinant PKCι phosphorylated at T411, which has high sequence similarity to the T560 region of PRKCZ

  • Sequential immunoprecipitation: Perform initial immunoprecipitation with isoform-specific antibodies followed by phospho-specific detection

  • Comparative phosphorylation analysis: Examine the phosphorylation ratio of phospho-T560-PKCζ/total-PKCζ versus phospho-T411-PKCι/total-PKCι to identify isoform-specific activation patterns

  • Data validation methodology:

    • Western blot analysis with isoform-specific antibodies

    • Parallel detection of PKCα, PKCβ, PKCγ, PKCδ, PKCε, PKCη, PKCθ, and PKCι using commercially available antibodies

    • Normalization to total protein within the 38-102 kDa range on Coomassie-stained gels

What methodological approaches are recommended for studying PRKCZ phosphorylation in NF-kappa-B signaling pathways?

Investigating PRKCZ phosphorylation in NF-kappa-B signaling requires specialized approaches:

  • Stimulation protocols:

    • Lipopolysaccharide (LPS) treatment in macrophages activates PRKCZ via PI3K

    • TNF-α stimulation for NF-kappa-B transactivation studies

    • Interleukin-1 signaling via SQSTM1/p62 adapter

  • Co-immunoprecipitation strategy:

    • Immunoprecipitate PRKCZ complexes with adapters RIPK1 and TRAF6

    • Probe for phosphorylated IKBKB to detect downstream activation

  • Temporal analysis:

    • Track phosphorylation kinetics (5, 15, 30, 60, 120 minutes post-stimulation)

    • Correlate with nuclear translocation of NF-kappa-B components

  • Inhibitor controls:

    • PI3K inhibitors (wortmannin, LY294002) to block upstream activation

    • PRKCZ-specific peptide inhibitors to confirm pathway specificity

How do findings from Prkcz knockout models inform phosphorylation studies?

Prkcz knockout models provide critical contextual information for phosphorylation studies:

  • Phenotypic observations:

    • Male Prkcz−/− mice show reduced anxiety-like behavior compared to wild-type mice

    • No significant differences in learning and memory were observed between Prkcz−/− and wild-type mice

  • Compensatory mechanisms:

    • Western blot analysis reveals no compensatory increase in phosphorylation of PKCι at T411 in Prkcz−/− mice

    • The ratio of phospho-T411-PKCι/total-PKCι immunoreactivity remained consistent across genotypes

  • Experimental design implications:

    • Include sex as a biological variable when studying PRKCZ phosphorylation, as phenotypic effects may be sex-dependent

    • Use statistical analysis that accounts for sex as a factor: F sex(1,22)=13.56, P=0.001; F genotype(1,22)=0.292, P=0.59

  • Validation methodology:

    • Quantify immunoreactive bands using ImageJ (http://rsbweb.nih.gov/ij/)

    • Normalize phospho-PKC samples to total protein detected on Coomassie Blue stained gels

What technical challenges arise when detecting transient phosphorylation events in PRKCZ signaling?

Capturing transient phosphorylation events presents unique technical challenges:

  • Rapid sample preservation:

    • Flash-freezing in liquid nitrogen immediately following stimulation

    • Use of UV-crosslinking to stabilize protein-protein interactions

  • Time-course optimization:

    • Design experiments with closely spaced time points (30 seconds, 1, 2, 5 minutes)

    • Include both early (seconds to minutes) and late (hours) time points to capture full activation dynamics

  • Subcellular fractionation approach:

    • Separate nuclear, cytoplasmic, and membrane fractions rapidly

    • Preserve phosphorylation status with phosphatase inhibitors throughout fractionation process

    • Analyze translocation between compartments as an indicator of activation

  • Signal amplification strategies:

    • Consider proximity ligation assays for detecting low abundance phosphorylated proteins

    • Use highly sensitive ECL substrates for Western blot detection

    • Employ fluorescence-based secondary antibodies with appropriate controls for quantification

How can researchers investigate the relationship between PRKCZ phosphorylation and its subcellular localization?

PRKCZ phosphorylation status affects its subcellular localization and function:

  • Co-localization analysis methodology:

    • Dual immunofluorescence with phospho-T560 PRKCZ antibody and markers for:

      • Cell polarity complexes (PARD6A)

      • Microtubule motors (dynein)

      • NF-kappa-B pathway components

      • Neuronal differentiation factors (FEZ1)

  • Dynamic translocation assessment:

    • Live-cell imaging with fluorescently tagged PRKCZ constructs

    • FRAP (Fluorescence Recovery After Photobleaching) analysis to measure mobility

    • Mutation of T560 to alanine or aspartic acid to assess phosphorylation dependency

  • Polarized cell models:

    • Use of migrating astrocytes to study CDC42-dependent recruitment

    • Neural progenitor cells for studying neuronal differentiation

    • Insulin-stimulated adipocytes for glucose transport studies

  • Quantification approaches:

    • Pearson's correlation coefficient for co-localization analysis

    • Line-scan intensity profiles across cellular compartments

    • 3D reconstruction of z-stack images to assess spatial distribution in complex tissues

Quick Inquiry

Personal Email Detected
Please use an institutional or corporate email address for inquiries. Personal email accounts ( such as Gmail, Yahoo, and Outlook) are not accepted. *

Category

Service

THE BIOTEK
THE BioTek is a global biotech company offering highly purified proteins for research in cancer, apoptosis, development, endocrinology, immunology, neuroscience, proteases, and stem cells.
  • Contact
  • Address: 1925 E Maple Ave, El Segundo, CA 90245 United States
  • Phone : +1 201-285-7826
  • Email : info@thebiotek.com
  • Hours : Mon.-Fri. 9:00 AM - 5:00 PM
© Copyright 2024 Thebiotek. All Rights Reserved.