2qxb - Revision history

OCA: Redirecting to 4lo9

2013-08-01T04:52:48Z

Redirecting to 4lo9

←Older revision		Revision as of 04:52, 1 August 2013
Line 1:		Line 1:
-	~~{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}~~	+	#REDIRECT [[4lo9]] This PDB entry is obsolete and replaced by 4lo9
-	~~===Human p53 Core Domain Mutant N235K===~~	+
-		+
-	~~==Disease==~~	+
-	[[~~http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN~~]] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[http://omim.org/entry~~/133239 133239]]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS~~ is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref> <ref>PMID:1933902</ref> <ref>PMID:1978757</ref> <ref>PMID:2259385</ref> <ref>PMID:1737852</ref> <ref>PMID:1565144</ref> <ref>PMID:7887414</ref> <ref>PMID:8825920</ref> <ref>PMID:9452042</ref> <ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[http://omim.org/entry/275355 275355]]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[http://omim.org/entry/211980 211980]]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[http://omim.org/entry/260500 260500]]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[http://omim.org/entry/202300 202300]]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[http://omim.org/entry/614740 614740]]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>	+
-		+
-	~~==Function==~~	+
-	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref> <ref>PMID:11025664</ref> <ref>PMID:12810724</ref> <ref>PMID:15186775</ref> <ref>PMID:15340061</ref> <ref>PMID:17317671</ref> <ref>PMID:17349958</ref> <ref>PMID:19556538</ref> <ref>PMID:20673990</ref> <ref>PMID:20959462</ref> <ref>PMID:22726440</ref>	+
-		+
-	~~==About this Structure==~~	+
-	[[2qxb]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].	+
-		+
-	~~==See Also==~~	+
-	*[[P53\|P53]]	+
-		+
-	~~==Reference==~~	+
-	~~<references group="xtra"/><references/>~~	+
-	~~[[Category: Homo sapiens]]~~	+
-	~~[[Category: Luecke, H.]]~~	+
-	~~[[Category: Wang, Y.]]~~	+
-	~~[[Category: Activator]]~~	+
-	~~[[Category: Anti-oncogene]]~~	+
-	~~[[Category: Apoptosis]]~~	+
-	~~[[Category: Cell cycle]]~~	+
-	~~[[Category: Crystal structure]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Dna-binding]]~~	+
-	~~[[Category: Endoplasmic reticulum]]~~	+
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Host-virus interaction]]~~	+
-	~~[[Category: Li-fraumeni syndrome]]~~	+
-	~~[[Category: Metal-binding]]~~	+
-	~~[[Category: Nucleus]]~~	+
-	~~[[Category: P53]]~~	+
-	~~[[Category: Phosphorylation]]~~	+
-	~~[[Category: Rescue]]~~	+
-	~~[[Category: Suppressor mutation]]~~	+
-	~~[[Category: Transcription]]~~	+
-	~~[[Category: Transcription regulation]]~~	+

OCA at 06:12, 16 May 2013

2013-05-16T06:12:06Z

←Older revision		Revision as of 06:12, 16 May 2013
Line 3:		Line 3:

	==Disease==		==Disease==
-	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[http://omim.org/entry/133239 133239]]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref><ref>PMID:1933902</ref><ref>PMID:1978757</ref><ref>PMID:2259385</ref><ref>PMID:1737852</ref><ref>PMID:1565144</ref><ref>PMID:7887414</ref><ref>PMID:8825920</ref><ref>PMID:9452042</ref><ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[http://omim.org/entry/275355 275355]]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[http://omim.org/entry/211980 211980]]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[http://omim.org/entry/260500 260500]]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[http://omim.org/entry/202300 202300]]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[http://omim.org/entry/614740 614740]]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>	+	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[http://omim.org/entry/133239 133239]]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref> <ref>PMID:1933902</ref> <ref>PMID:1978757</ref> <ref>PMID:2259385</ref> <ref>PMID:1737852</ref> <ref>PMID:1565144</ref> <ref>PMID:7887414</ref> <ref>PMID:8825920</ref> <ref>PMID:9452042</ref> <ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[http://omim.org/entry/275355 275355]]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[http://omim.org/entry/211980 211980]]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[http://omim.org/entry/260500 260500]]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[http://omim.org/entry/202300 202300]]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[http://omim.org/entry/614740 614740]]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>

	==Function==		==Function==
-	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref><ref>PMID:11025664</ref><ref>PMID:12810724</ref><ref>PMID:15186775</ref><ref>PMID:15340061</ref><ref>PMID:17317671</ref><ref>PMID:17349958</ref><ref>PMID:19556538</ref><ref>PMID:20673990</ref><ref>PMID:20959462</ref><ref>PMID:22726440</ref>	+	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref> <ref>PMID:11025664</ref> <ref>PMID:12810724</ref> <ref>PMID:15186775</ref> <ref>PMID:15340061</ref> <ref>PMID:17317671</ref> <ref>PMID:17349958</ref> <ref>PMID:19556538</ref> <ref>PMID:20673990</ref> <ref>PMID:20959462</ref> <ref>PMID:22726440</ref>

	==About this Structure==		==About this Structure==

OCA at 23:01, 24 March 2013

2013-03-24T23:01:44Z

←Older revision		Revision as of 23:01, 24 March 2013
Line 1:		Line 1:
-	[[Image:2qxb.png\|left\|200px]]
-
	{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}		{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}
-
	===Human p53 Core Domain Mutant N235K===		===Human p53 Core Domain Mutant N235K===

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Note=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. Defects in TP53 are a cause of esophageal cancer (ESCR) [MIM:[http://omim.org/entry/133239 133239]]. Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.<ref>PMID:10570149</ref><ref>PMID:1933902</ref><ref>PMID:1978757</ref><ref>PMID:2259385</ref><ref>PMID:1737852</ref><ref>PMID:1565144</ref><ref>PMID:7887414</ref><ref>PMID:8825920</ref><ref>PMID:9452042</ref><ref>PMID:10484981</ref> Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:[http://omim.org/entry/275355 275355]]; also known as squamous cell carcinoma of the head and neck. Defects in TP53 are a cause of lung cancer (LNCR) [MIM:[http://omim.org/entry/211980 211980]]. LNCR is a common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [MIM:[http://omim.org/entry/260500 260500]]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood.<ref>PMID:12085209</ref> Defects in TP53 are a cause of adrenocortical carcinoma (ADCC) [MIM:[http://omim.org/entry/202300 202300]]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.<ref>PMID:11481490</ref> Defects in TP53 are the cause of susceptibility to basal cell carcinoma 7 (BCC7) [MIM:[http://omim.org/entry/614740 614740]]. A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter.<ref>PMID:21946351</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/P53_HUMAN P53_HUMAN]] Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; te function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.<ref>PMID:9840937</ref><ref>PMID:11025664</ref><ref>PMID:12810724</ref><ref>PMID:15186775</ref><ref>PMID:15340061</ref><ref>PMID:17317671</ref><ref>PMID:17349958</ref><ref>PMID:19556538</ref><ref>PMID:20673990</ref><ref>PMID:20959462</ref><ref>PMID:22726440</ref>

	==About this Structure==		==About this Structure==
Line 11:		Line 13:
	==See Also==		==See Also==
	*[[P53\|P53]]		*[[P53\|P53]]
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Luecke, H.]]		[[Category: Luecke, H.]]

OCA at 20:22, 20 October 2012

2012-10-20T20:22:58Z

←Older revision		Revision as of 20:22, 20 October 2012
Line 7:		Line 7:

	==About this Structure==		==About this Structure==
-	[[2qxb]] is a 4 chain structure ~~of [[P53]]~~ with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].	+	[[2qxb]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].

	==See Also==		==See Also==

OCA: Protected "2qxb" [edit=sysop:move=sysop]

2012-07-27T10:18:01Z

Protected "2qxb" [edit=sysop:move=sysop]

←Older revision

Revision as of 10:18, 27 July 2012

OCA at 10:17, 27 July 2012

2012-07-27T10:17:59Z

←Older revision		Revision as of 10:17, 27 July 2012
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-	{{Seed}}
	[[Image:2qxb.png\|left\|200px]]		[[Image:2qxb.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_2qxb", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
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	{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}		{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}

Line 14:		Line 7:

	==About this Structure==		==About this Structure==
-	~~2QXB~~ is a 4 ~~chains~~ structure of ~~sequences~~ from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].	+	[[2qxb]] is a 4 chain structure of [[P53]] with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].
		+
		+	==See Also==
		+	*[[P53\|P53]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Luecke, H.]]		[[Category: Luecke, H.]]
	[[Category: Wang, Y.]]		[[Category: Wang, Y.]]
-	[[Category: Acetylation]]
	[[Category: Activator]]		[[Category: Activator]]
-	[[Category: Alternative splicing]]
	[[Category: Anti-oncogene]]		[[Category: Anti-oncogene]]
	[[Category: Apoptosis]]		[[Category: Apoptosis]]
	[[Category: Cell cycle]]		[[Category: Cell cycle]]
	[[Category: Crystal structure]]		[[Category: Crystal structure]]
-	[[Category: Cytoplasm]]
	[[Category: Disease mutation]]		[[Category: Disease mutation]]
	[[Category: Dna-binding]]		[[Category: Dna-binding]]
Line 36:		Line 29:
	[[Category: P53]]		[[Category: P53]]
	[[Category: Phosphorylation]]		[[Category: Phosphorylation]]
-	[[Category: Polymorphism]]
	[[Category: Rescue]]		[[Category: Rescue]]
	[[Category: Suppressor mutation]]		[[Category: Suppressor mutation]]
	[[Category: Transcription]]		[[Category: Transcription]]
	[[Category: Transcription regulation]]		[[Category: Transcription regulation]]
-	[[Category: Ubl conjugation]]
-	[[Category: Zinc]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Feb 18 04:02:36 2009''

OCA at 02:02, 18 February 2009

2009-02-18T02:02:37Z

←Older revision		Revision as of 02:02, 18 February 2009
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	{{Seed}}		{{Seed}}
-	[[Image:2qxb.~~jpg~~\|left\|200px]]	+	[[Image:2qxb.png\|left\|200px]]

	<!--		<!--
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	==About this Structure==		==About this Structure==
-	2QXB is a ~~[[Single protein]]~~ structure of ~~sequence~~ from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].	+	2QXB is a 4 chains structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Single protein]]
	[[Category: Luecke, H.]]		[[Category: Luecke, H.]]
	[[Category: Wang, Y.]]		[[Category: Wang, Y.]]
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	[[Category: Zinc]]		[[Category: Zinc]]

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed ~~Aug 27 11~~:06:~~50 2008~~''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Feb 18 04:02:36 2009''

OCA at 08:06, 27 August 2008

2008-08-27T08:06:51Z

←Older revision		Revision as of 08:06, 27 August 2008
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-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:2qxb.jpg\|left\|200px]]

-	The ~~entry 2qxb~~ is ~~ON HOLD~~ ~~until Aug 26 2009~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_2qxb", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_2qxb\| PDB=2qxb \| SCENE= }}

-	~~Authors: Luecke, H., Wang, Y.~~	+	===Human p53 Core Domain Mutant N235K===

-	Description: Human p53 Core Domain Mutant N235K

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Aug ~~13 13~~:32:44 2008''	+	==About this Structure==
		+	2QXB is a [[Single protein]] structure of sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2QXB OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Single protein]]
		+	[[Category: Luecke, H.]]
		+	[[Category: Wang, Y.]]
		+	[[Category: Acetylation]]
		+	[[Category: Activator]]
		+	[[Category: Alternative splicing]]
		+	[[Category: Anti-oncogene]]
		+	[[Category: Apoptosis]]
		+	[[Category: Cell cycle]]
		+	[[Category: Crystal structure]]
		+	[[Category: Cytoplasm]]
		+	[[Category: Disease mutation]]
		+	[[Category: Dna-binding]]
		+	[[Category: Endoplasmic reticulum]]
		+	[[Category: Glycoprotein]]
		+	[[Category: Host-virus interaction]]
		+	[[Category: Li-fraumeni syndrome]]
		+	[[Category: Metal-binding]]
		+	[[Category: Nucleus]]
		+	[[Category: P53]]
		+	[[Category: Phosphorylation]]
		+	[[Category: Polymorphism]]
		+	[[Category: Rescue]]
		+	[[Category: Suppressor mutation]]
		+	[[Category: Transcription]]
		+	[[Category: Transcription regulation]]
		+	[[Category: Ubl conjugation]]
		+	[[Category: Zinc]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Aug 27 11:06:50 2008''

OCA at 10:32, 13 August 2008

2008-08-13T10:32:44Z

←Older revision		Revision as of 10:32, 13 August 2008
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 2qxb is ON HOLD until ~~Paper Publication~~	+	The entry 2qxb is ON HOLD until Aug 26 2009

	Authors: Luecke, H., Wang, Y.		Authors: Luecke, H., Wang, Y.
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	Description: Human p53 Core Domain Mutant N235K		Description: Human p53 Core Domain Mutant N235K

-		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Aug 13 13:32:44 2008''
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed ~~Jun 11 08~~:39:34 2008''	+

OCA: New page: '''Unreleased structure''' The entry 2qxb is ON HOLD until Paper Publication Authors: Luecke, H., Wang, Y. Description: Human p53 Core Domain Mutant N235K ''Page seeded by [http://oc...

2008-06-11T05:39:35Z

New page: '''Unreleased structure''' The entry 2qxb is ON HOLD until Paper Publication Authors: Luecke, H., Wang, Y. Description: Human p53 Core Domain Mutant N235K ''Page seeded by [http://oc...

New page

'''Unreleased structure'''

The entry 2qxb is ON HOLD until Paper Publication

Authors: Luecke, H., Wang, Y.

Description: Human p53 Core Domain Mutant N235K

''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jun 11 08:39:34 2008''