Anti-Human CD45RO (Clone UCHL-1) – Purified in vivo Functional GOLD^TM Functional Grade

Clone UCHL-1 (commonly referred to as anti-CD45RO, clone UCHL-1) is most frequently employed in mice as a tool for tissue staining, immunohistochemistry, and immune cell marker detection, rather than as a functional agent for depletion or modulation in vivo.

Essential context and supporting details:

• UCHL-1 in Immunology: The clone UCHL-1 antibody is specific for human CD45RO (a marker of memory T cells) and is often utilized to identify human T cells in tissue sections through histological staining or flow cytometry, especially in xenograft or humanized mouse models.
• Functional Use: There is little evidence that UCHL-1 (CD45RO) antibody is used therapeutically, such as for depleting human T cell populations in vivo in mice. Its main value lies in tracking or visualizing specific immune cell populations after tissue harvest.

Additional relevant information:

• Mouse Reactivity: Clone UCHL-1 is not reactive to mouse CD45R (B220) or mouse CD45 antigens. Its applications in mice are therefore limited to experiments involving the detection of human cells introduced into mice (e.g., human T cell xenografts or adoptive transfer).
• Comparison with Other Antibodies: For depletion of mouse lymphocyte populations in vivo, researchers typically use other antibodies (e.g., anti-mouse CD45R/B220). Clone UCHL-1 is specific to the human isoform CD45RO and does not cross-react with mouse antigens.

If your question aimed at UCHL1 in the context of the ubiquitin hydrolase protein (not the CD45RO antibody), there are numerous in vivo studies in mice investigating the role of UCHL1 in neurobiology and disease (such as Alzheimer's models, ischemia, neurodegeneration, and neuroprotection). However, in those cases, "UCHL1" refers to the protein/enzyme, not the antibody clone. If you meant this second usage, please clarify.

In the literature, UCHL1 is often studied in conjunction with other proteins and antibodies, particularly in the context of its role as a deubiquitinating enzyme. Here are some commonly used antibodies or proteins associated with UCHL1:

1. Alpha-Synuclein: This protein is associated with Parkinson's disease and is deubiquitinated by UCHL1, which plays a role in maintaining synaptic function and possibly in neurodegenerative diseases.

2. Amyloid-Beta Precursor Protein (APP): UCHL1 is involved in regulating APP processing, which is crucial for amyloid-beta production in Alzheimer's disease.

3. p53: UCHL1 binds to p53 promoting its degradation, a process that can impact cancer progression.

4. E2F1: UCHL1 can stabilize nucleoporin POM121, leading to increased nuclear localization of E2F1, which is relevant in cancer contexts.

5. EGFR: UCHL1 deubiquitinates and stabilizes the epidermal growth factor receptor, preventing its degradation and activating downstream signaling pathways.

6. HIF1A: UCHL1 prevents the degradation of hypoxia-inducible factor 1-alpha by abrogating its ubiquitination, thus enhancing its activity.

Antibodies Used for UCHL1 Detection:

• While specific antibodies for UCHL1 detection are used, the literature often focuses on the functional roles of UCHL1 rather than detailing specific antibody types. Commonly, both monoclonal and polyclonal antibodies are used for research purposes.

Key findings from scientific literature citing clone UCHL-1 focus on two main areas: UCHL1 as a diagnostic and functional marker in cancer and neurobiology and clone UCHL-1’s role in identifying the CD45RO antigen on immune cells.

1. UCHL1 in Cancer and Neurodegeneration

• UCHL1 is highly expressed in neuroendocrine neoplasms and is detectable in patient plasma, making it a promising molecular biomarker for diagnosing neuroendocrine carcinomas and neuroblastoma, as well as monitoring therapy responses.
• Functional role in tumor progression: Loss of UCHL1 reduces tumor growth and metastasis in neuroendocrine carcinoma and small cell lung cancer. UCHL1 regulates key cancer pathways (E2F, MYC, mTOR) and directly interacts with proteins like p53 and POM121 to facilitate neuroendocrine differentiation and metastasis.
• UCHL1 as a promoter of metastasis: It destabilizes p53 and stabilizes POM121, promoting rapid nuclear import of oncogenic transcription factors. Overexpression drives metastatic colonization, while inhibition or genetic silencing dramatically reduces metastasis (especially to bone, liver, lungs, lymph nodes).
• Therapeutic potential: Treating neuroendocrine tumors with UCHL1 inhibitors—alone or with chemotherapy—delays growth and curbs metastasis, indicating strong therapeutic relevance.
• Role in HIF-1α regulation: UCHL1 acts as a deubiquitinating enzyme for HIF-1α; overexpression increases stability and activity of HIF-1α, which is involved in tumor metastasis and poor prognosis in several cancers.
• General neurobiology: Knockout or inhibition of UCHL1 results in neurodegenerative phenotypes and highlights UCHL1's essential role in nervous system maintenance.

2. Clone UCHL-1 and CD45RO Detection

• In immunology, clone UCHL-1 refers to a monoclonal antibody specific for the human CD45RO antigen (also called B220).
• CD45RO: This glycoprotein is a member of the protein tyrosine phosphatase family and serves as a marker for mature memory T cells, distinguishing them from naïve T cells in both research and clinical settings.
• The clone UCHL-1 antibody is widely used for flow cytometry and immunohistochemistry to identify and characterize T cell populations based on memory status.

Additional Relevant Findings

• UCHL1 interacts with cell cycle kinases (CDKs) and potentiates CDK/cyclin complex activity, suggesting a role in regulating cell proliferation via non-canonical mechanisms.
• Mutations in UCHL1 alter its enzymatic activity, influencing ubiquitin processing and further implicating UCHL1 in neurodegenerative disease and cancer biology.

In summary, clone UCHL-1 is pivotal both as a research antibody for immune cell phenotyping via CD45RO and as a molecular target/marker in cancer and neuroscientific research, with key findings supporting its diagnostic and therapeutic utility.

Dosing regimens for the antibody clone UCHL-1 (typically referring to anti-human CD45RO, UCHL1 clone) are not standardized across mouse models, varying by the experimental context, mouse strain, and tissue targeted. In fact, most mouse models manipulating UCHL1 levels do so by genetic modification (overexpression or knockout), not antibody administration, making "dosing" of the clone itself irrelevant in those settings.

Key details by use case

• Immunodetection applications (e.g., flow cytometry, immunohistochemistry, Western blot):

  • Doses of clone UCHL-1 used for labeling tissues or cells vary by protocol and supplier recommendations, often ranging from 0.1 to 10 µg per staining, but these are not standardized and are tailored to each experiment.

• In vivo functional studies:

  • Transgenic/knockout models: UCHL1 activity in mice is mainly manipulated by genetic engineering, not exogenous antibody dosing.
  • Pharmacological inhibition (not directly by the UCHL-1 antibody clone, but by small-molecule inhibitors like LDN57444):
    • Example: LDN57444 has been used in some rodent models at 0.5 mg/kg/day, intraperitoneally.
    • These inhibitors—unlike antibody clones—are suitable for in vivo systemic modulation of UCHL1 activity.

Model-specific considerations

• Genetic knockout mice: Dosing of UCHL-1 antibody is not applicable; phenotypes observed are due to absence of UCHL1 protein.
• Transgenic overexpression models: No dosing regimen for clone; effects are due to genetic manipulation.
• Antibody-based regimens: Where used for labeling, doses must be empirically optimized for each tissue and detection system.

Summary Table

There is no universal dosing for clone UCHL-1 in murine models, as its application is generally limited to ex vivo detection rather than in vivo modulation, with actual dose choices varying by assay and research aim. Where systemic UCHL1 function is modulated, this is almost always by genetic or small-molecule approaches rather than antibody dosing.