PDLIM2 Antibody, Biotin conjugated

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Description

Applications in Research

The biotin-conjugated PDLIM2 antibody is primarily used in:

  • ELISA: For quantifying PDLIM2 protein levels in lysates or tissue extracts.

  • IHC: To localize PDLIM2 expression in fixed tissue sections (e.g., lung cancer biopsies).

  • Western Blotting: When paired with streptavidin-HRP or streptavidin-alkaline phosphatase for signal detection.

Key Research Context:
PDLIM2 is a tumor suppressor that represses STAT3 and RelA, limiting tumor-promoting macrophage activation in lung cancer . Its downregulation correlates with poor prognosis in patients . This antibody facilitates studies on PDLIM2’s role in immune modulation and therapeutic resistance.

Suppliers and Availability

SupplierProduct CodeKey Features
Abbexa LtdPDLIM2 Antibody (Biotin)Rabbit polyclonal, human-specific, ELISA-validated
CusabioCSB-PA856962LD01HUBiotin conjugate for ELISA
Novus BiologicalsNBP2-00619COVID-19 research tools

Notes:

  • Abbexa’s product is optimized for ELISA with a recommended dilution of 1:20–1:200 for IHC .

  • Cusabio offers conjugation flexibility (HRP, FITC, Biotin) for diverse protocols .

Data Table: Recommended Dilutions

ApplicationDilution RangeSource
ELISA1:1,000–1:10,000
IHC1:20–1:200

Product Specs

Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
We typically dispatch orders within 1-3 business days of receipt. Delivery times may vary depending on the purchase method and location. Please consult your local distributor for specific delivery details.
Synonyms
FLJ34715 antibody; MYSTIQUE antibody; OTTHUMP00000162522 antibody; OTTHUMP00000205197 antibody; OTTHUMP00000205198 antibody; OTTHUMP00000205199 antibody; OTTHUMP00000205200 antibody; OTTHUMP00000205202 antibody; OTTHUMP00000205203 antibody; PDLI2_HUMAN antibody; Pdlim2 antibody; PDZ and LIM domain 2 (mystique) antibody; PDZ and LIM domain protein 2 antibody; PDZ-LIM protein mystique antibody; SLIM antibody; Stat-interacting LIM protein antibody
Target Names
PDLIM2
Uniprot No.

Target Background

Function
PDLIM2 is a probable adapter protein localized to the actin cytoskeleton. It plays a crucial role in promoting cell attachment and is essential for the migratory capacity of epithelial cells. Overexpression of PDLIM2 enhances cell adhesion to collagen and fibronectin while suppressing anchorage-independent growth. This suggests that PDLIM2 may contribute to the migratory capabilities of tumor cells.
Gene References Into Functions
  1. Our research demonstrated that (i) the use of SPR chips yielded comparable data to on-column streptavidin beads, (ii) gravity flow and microflow during wash and elution steps provided better results than centrifugation, and (iii) the type and concentration of detergent did not significantly impact the interactome data of cancer-associated PDLIM2. PMID: 30194080
  2. Our findings indicate that inactivation of PDLIM2 is a recurring feature in cHL and ALCL. This inactivation promotes the activation of inflammatory signaling pathways, contributing to the pathogenesis of these diseases. PMID: 27538486
  3. Our data show that shRNA-mediated knockdown of PDZ and LIM domain protein 2 (PDLIM2) in both primary meningioma and schwannoma leads to significant reductions in cellular proliferation. PMID: 28126595
  4. PDLIM2 is epigenetically repressed during ovarian cancer development. Inhibition of PDLIM2 promotes ovarian cancer growth both in vivo and in vitro through NOS2-derived nitric oxide signaling, leading to the recruitment of M2 type macrophages. PMID: 26593252
  5. The suppression of PDLIM2 expression significantly reduced cell proliferation, cell growth, and neoplasm invasiveness in prostate cancer cells. PMID: 26499308
  6. Epigenetic repression of PDLIM2 can be reversed by 5-aza-2-deoxycytidine and vitamin D to suppress KSHV-associated cancer cell growth. PMID: 25681443
  7. PDLIM2 expression is essential for feedback regulation of the beta1-integrin-RhoA signaling axis and integration of cellular microenvironment signals with gene expression to control the polarity of breast epithelial acini structures. PMID: 24863845
  8. PDLIM2 integrates cytoskeleton signaling with gene expression in epithelial differentiation by controlling the stability of key transcription factors and COP9 signalosome activity. PMID: 24196835
  9. PDLIM2 was a direct target gene of 1,25(OH)2D3. PMID: 23584482
  10. Pdlim2 is a novel actin-regulating protein of podocyte foot processes that may play a role in the pathogenesis of glomerular diseases. PMID: 21814175
  11. PDLIM2 binds directly to Tax, mediated by a putative alpha-helix motif of PDLIM2 at amino acids 236-254. PMID: 20838382
  12. PDLIM2, an essential terminator of NF-kappaB activation, is repressed in both estrogen receptor-positive and estrogen receptor-negative breast cancer cells, suggesting a crucial mechanism for the constitutive activation of NF-kappaB. PMID: 20185823
  13. Our data show that the PDLIM2 repression was independent of the viral regulatory protein Tax, as neither short-term induction nor long-term stable expression of Tax could downregulate PDLIM2 expression. PMID: 19794962
  14. Knockdown of Mystique 2 with small interfering RNA abrogated both adhesion and migration in MCF10A and MCF-7 cells. PMID: 15659642
  15. PDLIM2 deficiency resulted in larger amounts of nuclear p65, defective p65 ubiquitination, and augmented production of proinflammatory cytokines in response to innate stimuli. PMID: 17468759
  16. Suppression of PDLIM2 expression led to decreased cell adhesion, increased NF-kappaB transcription reporter activity, and increased LPS-induced TNF-alpha production. PMID: 19052146

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Database Links

HGNC: 13992

OMIM: 609722

KEGG: hsa:64236

STRING: 9606.ENSP00000312634

UniGene: Hs.632034

Subcellular Location
Cytoplasm. Nucleus. Note=May be partially nuclear.; [Isoform 1]: Cytoplasm, cytoskeleton. Note=Colocalizes with beta-1 integrin (ITGB1) and alpha-actinin but not with paxillin (PXN).; [Isoform 2]: Cytoplasm, cytoskeleton.; [Isoform 3]: Nucleus.

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