Leukemia Inhibitor Factor
Leukemia Inhibitor Factor - Related Videos
10:49
Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
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Cited by 6 •
2013
Receptor tyrosine kinases are ectopically expressed in many cancers and have been identified as therapeutic targets in acute leukemia. This manuscript describes an efficient strategy for pre-clinical evaluation of tyrosine kinase inhibitors for the treatment of acute leukemia.
08:31
Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia
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2025
The protocol aims to describe a mouse model for generating relapses of acute lymphoblastic leukemia, based on the dynamics of the response to induction chemotherapy.
01:52
Eukaryotic Transcription Inhibitors
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2020
Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells. Eukaryotic transcription inhibitors usually contain two distinct domains, a DNA...
02:57
G-10 Column Based Leukemia Cell Sorting: A Method to Purify Acute Lymphoblastic Leukemia Cells from Bone Marrow Stromal Cells
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2023
This video describes the separation of acute lymphoblastic leukemia cells from bone marrow stromal cells using gel-type ten cross-linked dextran G-10 columns. This method helps recover the population of tumor cells that have migrated beneath the adherent bone marrow stromal cells generating a "phase dim" tumor cell population.
09:06
Isolation of the Side Population in Myc-induced T-cell Acute Lymphoblastic Leukemia in Zebrafish
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Cited by 5 •
2017
Here, we describe a technique to isolate the side population cells from a zebrafish model of myc-induced T-cell acute lymphoblastic leukemia (T-ALL). This side population assay is highly sensitive and is described for zebrafish T-ALL, but it may be applicable to other malignant and non-malignant zebrafish cell types.
FAQs
Binding of LIF to its receptor and gp130 initiates intracellular signaling rather than acting only at the cell surface. JAK/STAT3 provides a central signaling route, while related pathways can also contribute. These signals modify gene expression, and the resulting changes help determine whether cells survive, proliferate, differentiate, or adopt developmental behaviors.
gp130 is a required signaling partner in the LIF receptor system. Its participation connects receptor engagement with JAK/STAT3 and related intracellular pathways, translating an extracellular cytokine cue into altered gene expression. Because these downstream changes influence several cellular behaviors, gp130 helps explain how one signaling system can produce broad biological effects.
Within certain embryonic stem-cell contexts, LIF supports self-renewal, allowing cells to retain an undifferentiated state. At the same time, LIF is linked to differentiation control, so its effect must be interpreted in relation to the surrounding signaling environment. This makes the cytokine useful for studying how external cues shape stem-cell fate.
LIF responses vary with the cellular and tissue setting, including the developmental or disease context in which signaling occurs. The same broad signaling capacity can therefore support survival or proliferation in one situation while participating in differentiation, inflammation, or tissue development in another. This dependence means LIF should not be assigned one universal cellular outcome.
LIF is relevant because it supports implantation, placing cytokine signaling within the biological events that establish early developmental interactions with tissue. Studying its receptor-mediated effects can help researchers connect changes in gene expression and cellular behavior with implantation-related processes. This context also illustrates why LIF research extends beyond isolated cell survival or proliferation.
LIF connects these areas through its influence on embryonic stem-cell self-renewal, differentiation, and tissue development. Research can therefore examine how signaling environments preserve stem-cell properties or alter developmental behavior, providing biological context for regenerative medicine. Its value lies in linking molecular signaling with the cellular decisions required for tissue formation and repair-oriented research.
Cancer research examines LIF because its signaling can affect cell survival, proliferation, differentiation, and disease progression. These effects are context-dependent, so investigators can study how altered signaling environments influence tumor-related cellular behavior rather than assuming one fixed outcome. LIF also provides a way to connect cytokine-mediated gene regulation with broader mechanisms of disease biology.
LIF research can address how cytokine signaling coordinates inflammatory responses while also influencing tissue development. Comparing these settings helps clarify how receptor-driven changes in gene expression produce different biological outcomes across tissues and stages. This broader perspective is important because LIF operates at the intersection of immune regulation, development, and context-sensitive cellular behavior.