Diamond Davis

Lab Sec 003

Homework 2
3/21/14
1. Bone morphogenetic proteins (BMPs) interact with the specific receptor bone morphogenetic
protein receptors (BMPRs). BMP play a important role in heart, neural, cartilage development,
and postnatal bone formation. BMP is also expressed in a wide variety of tissues including small
intestine, spleen, lung, prostate, and ovary (3). BMPs are produced by osteoblasts and other
bone cells (6).
2. BMP ligands bind to the BMP receptors BMPRI and BMPRII. BMPRII phosphorylates which
activates BMRI. The phosphorylated BMPRI phosphorylates Smad proteins( R- Smads) which
leads to common mediator Smad (Co-Smad) (7). Co-Smad enters the nucleus, binds to DNA,
associates with transcription factors, and regulates gene expression (4).
3. Cyclin-dependent kinases (CDKs) are versatile enzymes that can modify many different
protein substrates that are involved in the cell cycle. CDKs require cyclins to become active.
Cyclins are proteins that bind to CDKs to activate them (2). Cyclin E/CDK2 play an important
role in the G1-S phase transition. Cyclin E/CDK2 phosphorylates the protein retinoblastoma (Rb)
to promote the progression of G1 (5). Cyclin A/CDK2 has a major role in the S phase to G2
phase, it initiates and completes DNA replication. It also ensures the DNA is replicated only
once per cell cycle (1).
4. There are three major mechanisms for the activity of a tumor suppressor, suppression of cell
division, induction of apoptosis, and DNA damage repair (8). Suppression of cell division is the
main mechanism for a lot of tumor suppressors. Different tumor suppressors that use this
mechanism use it in various ways. Rb and p53 both inhibit specific genes that are necessary for

Diamond Davis
Lab Sec 003
Homework 2
3/21/14
mitosis by binding to transcription factors (8). Apoptosis which is a programmed cell death is
another mechanism for tumor suppressors, which is utilized by p53 as well (8). p53 can also
help in DNA damage repair. DNA damage repair involves fixing mismatch bases and breaks in
the DNA strand.

Works Cited
1. Bendris, Nawal, Bndicte Lemmers, Jean-Marie Blanchard, and Nikola Arsic. "Cyclin A2
Mutagenesis Analysis: A New Insight into CDK Activation and Cellular Localization
Requirements." Ed. Jean-Marc Vanacker. PLoS ONE 6.7 (2011): E22879. Web.
2. Carroll, John. "CDK." Nature.com. Nature Publishing Group, n.d. Web. 21 Mar. 2014.
3. Chen, Di, Ming Zhao, and Gregory R. Mundy. "Bone Morphogenetic Proteins." Growth
Factors 22.4 (2004): 233-41. Web.
4. Heldin, Carl-Henrik, and Aristidis Moustakas. "A New Twist in Smad Signaling."
Developmental Cell 10.6 (2006): 685-86. Web.
5. Hinds, Philip W., Sibylle Mittnacht, Vjekoslav Dulic, Andrew Arnold, Steven I. Reed, and
Robert A. Weinberg. "Regulation of Retinoblastoma Protein Functions by Ectopic
Expression of Human Cyclins." Cell 70.6 (1992): 993-1006. Web.
6. Linkhart, Thomas A., Subburaman Mohan, and David J. Baylink. "Growth Factors for Bone
Growth and Repair: IGF, TGF and BMP." Bone 19.1 (1996): S1-S12. Web.
7. Liu, Aimin, and Lee A. Niswander. "Bone Morphogenetic Protein Signalling and Vertebrate
Nervous System Development." Nature Reviews Neuroscience 6.12 (2005): 945-54. Web.

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8. Wanpeng Sun, Jian Yang. "Functional Mechanisms for Human Tumor Suppressors."
Functional Mechanisms for Human Tumor Suppressors. N.p., n.d. Web. 21 Mar. 2014.