CDKN1B: Difference between revisions

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'''CDKN1B''' (Cyclin-Dependent Kinase Inhibitor 1B), also known as '''p27Kip1''', is a protein that in humans is encoded by the ''CDKN1B'' gene. It plays a crucial role in regulating the [[cell cycle]], acting as a [[cell cycle checkpoint|checkpoint inhibitor]] to prevent cell proliferation by inhibiting [[cyclin-dependent kinases]] (CDKs). The importance of CDKN1B in controlling cell division makes it a key player in the development and progression of [[cancer]], as well as a potential target for cancer therapy.
== CDKN1B ==


==Function==
[[File:Signal_transduction_v1.png|thumb|right|Signal transduction pathways are crucial for cell cycle regulation.]]
CDKN1B is a member of the Cip/Kip family of cyclin-dependent kinase inhibitors. It binds to and inhibits the activity of cyclin-CDK2 or cyclin-CDK4 complexes, and thus functions as a regulator of [[cell cycle progression]] at G1. The activity of CDKN1B is regulated by its phosphorylation. Its high levels in the cell contribute to the arrest of the cell cycle in the G1 phase, making it a critical regulator of cell cycle entry and a potent inhibitor of cell proliferation.


==Gene and Expression==
'''CDKN1B''' (Cyclin-Dependent Kinase Inhibitor 1B), also known as '''p27^Kip1''', is a protein that in humans is encoded by the '''CDKN1B''' gene. It is a member of the [[cyclin-dependent kinase inhibitor]] family and plays a critical role in regulating the cell cycle.
The ''CDKN1B'' gene is located on chromosome 12p13.1-p12 in humans. Its expression is tightly controlled by various mechanisms, including transcriptional, post-transcriptional, and post-translational modifications. Alterations in the expression or function of CDKN1B have been implicated in the pathogenesis of a wide range of human cancers.


==Clinical Significance==
== Function ==
Alterations in CDKN1B, such as mutations, deletions, or reduced expression, have been associated with various types of cancer, including breast cancer, prostate cancer, and lymphoma. The loss of CDKN1B function contributes to uncontrolled cell proliferation, a hallmark of cancer. Additionally, CDKN1B has been studied for its potential role in other diseases characterized by abnormal cell cycle regulation.


==Cancer Therapy==
CDKN1B functions as a key regulator of the cell cycle by inhibiting the activity of [[cyclin-dependent kinase]]s (CDKs). It binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell's progression from the G1 phase to the S phase. This inhibition is crucial for maintaining proper cell cycle checkpoints and preventing uncontrolled cell proliferation.
Given its role in inhibiting cell proliferation, CDKN1B is considered a potential target for cancer therapy. Strategies to increase the expression or activity of CDKN1B could potentially halt the progression of tumors by arresting cancerous cells in the G1 phase of the cell cycle. Research is ongoing to develop drugs that can modulate the activity of CDKN1B for therapeutic purposes.


==Research Directions==
== Mechanism of Action ==
Research on CDKN1B continues to explore its role in cell cycle regulation, its mechanisms of action, and its involvement in cancer and other diseases. Understanding the complex regulation of CDKN1B and its interactions with other cell cycle regulators is crucial for developing novel therapeutic strategies targeting cell cycle dysregulation in cancer.


[[Category:Cell cycle]]
The protein encoded by CDKN1B acts as a tumor suppressor by controlling cell cycle progression. It is involved in the [[signal transduction]] pathways that respond to external growth signals. When growth signals are absent, CDKN1B accumulates in the nucleus and inhibits CDK activity, leading to cell cycle arrest.
[[Category:Genes]]
[[Category:Cancer research]]
{{Medicine-stub}}


==External Links==
[[File:Signal_transduction_v1.png|thumb|left|Signal transduction pathways involving CDKN1B.]]
* [https://www.ncbi.nlm.nih.gov/gene/1027 NCBI Gene: CDKN1B]
* [https://www.uniprot.org/uniprot/P46527 UniProt: P46527 (CDKN1B_HUMAN)]


==References==
== Clinical Significance ==
<references/>


==Images==
Mutations or alterations in the expression of CDKN1B have been associated with various types of cancer. Loss of function or reduced expression of CDKN1B can lead to unchecked cell division and tumor development. Conversely, overexpression of CDKN1B can result in cell cycle arrest and may be used as a therapeutic strategy in cancer treatment.
Images related to CDKN1B can be found on Wikimedia Commons:
* [https://commons.wikimedia.org/wiki/Category:CDKN1B Wikimedia Commons: Category:CDKN1B]


Please note that while this article provides a comprehensive overview of CDKN1B, including its function, clinical significance, and potential as a therapeutic target, the field of cancer research is rapidly evolving. New discoveries and technologies continue to shed light on the complex biology of cancer and the role of key regulators like CDKN1B.
== Regulation ==
 
CDKN1B is regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational modifications. Phosphorylation of CDKN1B can lead to its degradation via the ubiquitin-proteasome pathway, thus modulating its inhibitory effects on the cell cycle.
 
== Related Pages ==
 
* [[Cell cycle]]
* [[Cyclin-dependent kinase]]
* [[Tumor suppressor gene]]
* [[Signal transduction]]
 
[[Category:Cell cycle regulators]]
[[Category:Tumor suppressor genes]]

Latest revision as of 11:01, 15 February 2025

CDKN1B[edit]

Signal transduction pathways are crucial for cell cycle regulation.

CDKN1B (Cyclin-Dependent Kinase Inhibitor 1B), also known as p27^Kip1, is a protein that in humans is encoded by the CDKN1B gene. It is a member of the cyclin-dependent kinase inhibitor family and plays a critical role in regulating the cell cycle.

Function[edit]

CDKN1B functions as a key regulator of the cell cycle by inhibiting the activity of cyclin-dependent kinases (CDKs). It binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell's progression from the G1 phase to the S phase. This inhibition is crucial for maintaining proper cell cycle checkpoints and preventing uncontrolled cell proliferation.

Mechanism of Action[edit]

The protein encoded by CDKN1B acts as a tumor suppressor by controlling cell cycle progression. It is involved in the signal transduction pathways that respond to external growth signals. When growth signals are absent, CDKN1B accumulates in the nucleus and inhibits CDK activity, leading to cell cycle arrest.

Signal transduction pathways involving CDKN1B.

Clinical Significance[edit]

Mutations or alterations in the expression of CDKN1B have been associated with various types of cancer. Loss of function or reduced expression of CDKN1B can lead to unchecked cell division and tumor development. Conversely, overexpression of CDKN1B can result in cell cycle arrest and may be used as a therapeutic strategy in cancer treatment.

Regulation[edit]

CDKN1B is regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational modifications. Phosphorylation of CDKN1B can lead to its degradation via the ubiquitin-proteasome pathway, thus modulating its inhibitory effects on the cell cycle.

Related Pages[edit]