Datasheet

生物学的記述

Specificity	TPX2 Antibody (Rabbit mAb) [C1B23] detects endogenous levels of total TPX2 protein.
Background	Targeting protein for Xklp2 (TPX2) is a Ran-regulated microtubule-associated protein that localizes to the nucleus in interphase and to spindle microtubules during mitosis, where it functions as a key factor for spindle assembly, chromosome segregation and maintenance of genomic stability in dividing cells. The protein contains multiple coiled-coil and microtubule-binding regions and a C‑terminal Aurora A–activating domain; TPX2 binds and activates Aurora A kinase, protects it from dephosphorylation and targets it to spindle microtubules, thereby coordinating microtubule nucleation, stabilization and centrosome-independent spindle formation in a RanGTP-dependent manner. TPX2 also interacts with kinesin motors such as Xklp2 and Eg5, integrating motor activity with microtubule dynamics to ensure bipolar spindle formation and proper alignment of chromosomes at metaphase. In hepatocellular carcinoma, TPX2 is highly expressed in tumor tissues compared with adjacent non-tumoral liver, and elevated TPX2 correlates with poor prognosis; siRNA-mediated knockdown of TPX2 in HCC cell lines reduces cell growth, induces G2/M arrest, promotes apoptosis and inhibits epithelial–mesenchymal transition, demonstrating that TPX2 supports proliferation, survival and invasive behavior in these tumors. Detailed analysis of TPX2-depleted HCC cells shows increased levels of pro-apoptotic and DNA damage–related proteins including Bax, p53, caspase‑3 and caspase‑8, together with upregulation of the epithelial marker E‑cadherin and downregulation of N‑cadherin, β‑catenin, MMP‑2, MMP‑9 and the EMT transcription factor Slug, indicating that TPX2 influences cell-cycle and apoptotic machinery and modulates EMT-associated signaling networks. TPX2 knockdown also reduces phosphorylation of Akt and ERK, linking TPX2-dependent mitotic functions to activation of PI3K/Akt and MAPK pathways that drive tumor formation and progression in HCC. Across multiple solid tumors including colon, gastric and endometrial cancers, TPX2 overexpression is consistently associated with high proliferative indices, increased metastasis and poor survival, and integrative analyses identify TPX2-centered co-expression networks and TPX2/TTK mitotic checkpoint modules as key drivers of aggressive disease, making TPX2 a robust proliferation- and mitosis-related biomarker.

Specificity

TPX2 Antibody (Rabbit mAb) [C1B23] detects endogenous levels of total TPX2 protein.

Background

Targeting protein for Xklp2 (TPX2) is a Ran-regulated microtubule-associated protein that localizes to the nucleus in interphase and to spindle microtubules during mitosis, where it functions as a key factor for spindle assembly, chromosome segregation and maintenance of genomic stability in dividing cells. The protein contains multiple coiled-coil and microtubule-binding regions and a C‑terminal Aurora A–activating domain; TPX2 binds and activates Aurora A kinase, protects it from dephosphorylation and targets it to spindle microtubules, thereby coordinating microtubule nucleation, stabilization and centrosome-independent spindle formation in a RanGTP-dependent manner. TPX2 also interacts with kinesin motors such as Xklp2 and Eg5, integrating motor activity with microtubule dynamics to ensure bipolar spindle formation and proper alignment of chromosomes at metaphase. In hepatocellular carcinoma, TPX2 is highly expressed in tumor tissues compared with adjacent non-tumoral liver, and elevated TPX2 correlates with poor prognosis; siRNA-mediated knockdown of TPX2 in HCC cell lines reduces cell growth, induces G2/M arrest, promotes apoptosis and inhibits epithelial–mesenchymal transition, demonstrating that TPX2 supports proliferation, survival and invasive behavior in these tumors. Detailed analysis of TPX2-depleted HCC cells shows increased levels of pro-apoptotic and DNA damage–related proteins including Bax, p53, caspase‑3 and caspase‑8, together with upregulation of the epithelial marker E‑cadherin and downregulation of N‑cadherin, β‑catenin, MMP‑2, MMP‑9 and the EMT transcription factor Slug, indicating that TPX2 influences cell-cycle and apoptotic machinery and modulates EMT-associated signaling networks. TPX2 knockdown also reduces phosphorylation of Akt and ERK, linking TPX2-dependent mitotic functions to activation of PI3K/Akt and MAPK pathways that drive tumor formation and progression in HCC. Across multiple solid tumors including colon, gastric and endometrial cancers, TPX2 overexpression is consistently associated with high proliferative indices, increased metastasis and poor survival, and integrative analyses identify TPX2-centered co-expression networks and TPX2/TTK mitotic checkpoint modules as key drivers of aggressive disease, making TPX2 a robust proliferation- and mitosis-related biomarker.

使用情報

Application

WB, IHC, IF, FCM

Dilution

WB	IHC	IF	FCM
1:1000	1:1000	1:50	1:50

Reactivity

Mouse, Rat, Human

Source

Rabbit Monoclonal Antibody

MW

86 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/28069036/
https://pubmed.ncbi.nlm.nih.gov/24556998/

TPX2 Antibody (Rabbit mAb) [C1B23]

生物学的記述

使用情報

References

Application Data