Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

Differentiation of Common Myeloid Progenitor Cells

Differentiation of Common Myeloid Progenitor Cells

Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...

T Cell Activation and Clonal Selection

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Identification of the gene cluster for the dithiolopyrrolone antibiotic holomycin in Streptomyces clavuligerus.

Proceedings of the National Academy of Sciences of the United States of America·2010

Same author

Safety evaluation of tea (Camellia sinensis (L.) O. Kuntze) flower extract: assessment of mutagenicity, and acute and subchronic toxicity in rats.

Journal of ethnopharmacology·2010

Same author

Influences of soil properties and leaching on nickel toxicity to barley root elongation.

Ecotoxicology and environmental safety·2010

Same author

Effects of CO2 insufflation on cerebrum during endoscopic thyroidectomy in a porcine model.

Surgical endoscopy·2010

Same author

Plants' use of different nitrogen forms in response to crude oil contamination.

Environmental pollution (Barking, Essex : 1987)·2010

Same author

Overexpression of p35 in Min6 pancreatic beta cells induces a stressed neuron-like apoptosis.

Journal of the neurological sciences·2010

Search research articles

Related Experiment Video

Updated: May 16, 2026

Pan-myeloid Differentiation of Human Cord Blood Derived CD34+ Hematopoietic Stem and Progenitor Cells

Pan-myeloid Differentiation of Human Cord Blood Derived CD34⁺ Hematopoietic Stem and Progenitor Cells

Published on: August 9, 2019

BCL11B suppression does not influence CD34(+) cell differentiation and proliferation.

Qi Shen¹, Xin Huang, Si Chen

¹Institute of Hematology, Medical College, Jinan University, Guangzhou, PR China.

Hematology (Amsterdam, Netherlands)

|November 22, 2012

Summary

BCL11B gene suppression using BCL11B-siRNA935 did not affect hematopoietic stem/progenitor cell differentiation or proliferation. This suggests BCL11B-siRNA935 is safe for potential targeted gene therapy in T-cell malignancies.

More Related Videos

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Published on: March 4, 2015

Related Experiment Videos

Last Updated: May 16, 2026

Pan-myeloid Differentiation of Human Cord Blood Derived CD34+ Hematopoietic Stem and Progenitor Cells

Pan-myeloid Differentiation of Human Cord Blood Derived CD34⁺ Hematopoietic Stem and Progenitor Cells

Published on: August 9, 2019

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Published on: March 4, 2015

Area of Science:

Hematology
Molecular Biology
Gene Therapy

Background:

The BCL11B gene is crucial for T-cell development and proliferation.
Its role in human hematopoietic stem/progenitor cells remains largely unknown.
BCL11B suppression via siRNA induces apoptosis in T-cell acute lymphoblastic leukemia cells.

Purpose of the Study:

To investigate the function of BCL11B in human hematopoietic stem/progenitor cells.
To evaluate the safety of BCL11B-siRNA935 for targeted gene therapy.

Main Methods:

CD34(+) cells were isolated from umbilical cord blood.
BCL11B expression was suppressed using BCL11B-siRNA935 via nucleofection.
Cell differentiation and proliferation were assessed using colony formation assays (BFU-E, CFU-GM, CFU-Meg).

Main Results:

BCL11B mRNA levels were reduced by approximately 50% 24 hours post-transfection.
No significant differences were observed in the colony-forming ability of BFU-E, CFU-GM, or CFU-Meg between treated and control groups.
BCL11B suppression did not impact CD34(+) cell differentiation or proliferation.

Conclusions:

BCL11B-siRNA935 treatment did not significantly affect hematopoietic stem/progenitor cell differentiation and proliferation.
BCL11B-siRNA935 appears safe for use in CD34(+) cells.
BCL11B is a potential candidate for targeted gene therapy in T-cell malignancies.